Volume 10, Issue 12

Maiuri L, Kroemer G, . Autophagy delays progression of the two most frequent human monogenetic lethal diseases: cystic fibrosis and Wilson disease. . 10:3657-3661. https://doi.org/10.18632/aging.101736

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                TY  - JOUR
                AU  - Maiuri, Luigi 
                AU  - Kroemer, Guido 
                TI  - Autophagy delays progression of the two most frequent human monogenetic lethal diseases: cystic fibrosis and Wilson disease
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101736
                DO  - 10.18632/aging.101736
                SP  - 3657
                EP  - 3661
                PY  - 
                AB  - Cystic fibrosis (CF) and Wilson disease (WD) are two monogenetic, recessively inherited lethal pathologies that are caused by ionic disequilibria. CF results from loss-of-function mutations in CF transmembrane conductance regulator (CFTR), a channel that conducts chloride across epithelial cell membranes, while WD is due to a deficiency of ATPase copper transporting beta (ATP7B), a plasma membrane protein that pumps out copper from cells. Recent evidence suggests that both diseases are linked to perturbations in autophagy. CFTR deficiency causes an inhibition of autophagic flux, thus locking respiratory epithelial cells in a pro-inflammatory state and subverting the bactericidal function of macrophages. WD is linked to an increase in autophagy, which, however, is insufficient to mitigate the cytotoxicity of copper. Pharmacological induction of autophagy may delay disease progression, as indicated by preclinical evidence (for CF and WD) and results from clinical trials, in particular in CF patients with the most frequent CTRT mutation (CFTRdel506). Thus, CF and WD exemplify pathologies in which insufficient autophagy plays a major role in determining the chronology of disease progression, much like the pace of ‘normal’ aging that is dictated by disabled autophagy as well.
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Long noncoding RNA B3GALT5-AS1 suppresses colon cancer liver metastasis via repressing microRNA-203

Liang Wang, Zhewei Wei, Kaiming Wu, Weigang Dai, Changhua Zhang, Jianjun Peng, Yulong He,

https://doi.org/10.18632/aging.101628 pp 3662—3682

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Wang L, Wei Z, Wu K, Dai W, Zhang C, Peng J, He Y, . Long noncoding RNA B3GALT5-AS1 suppresses colon cancer liver metastasis via repressing microRNA-203. . 10:3662-3682. https://doi.org/10.18632/aging.101628

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                TY  - JOUR
                AU  - Wang, Liang 
                AU  - Wei, Zhewei 
                AU  - Wu, Kaiming 
                AU  - Dai, Weigang 
                AU  - Zhang, Changhua 
                AU  - Peng, Jianjun 
                AU  - He, Yulong 
                TI  - Long noncoding RNA B3GALT5-AS1 suppresses colon cancer liver metastasis via repressing microRNA-203
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101628
                DO  - 10.18632/aging.101628
                SP  - 3662
                EP  - 3682
                PY  - 
                AB  - Long noncoding RNAs (lncRNAs) are implicated in various cancers, including colon cancer. Liver metastasis is the main cause of colon cancer-related death. However, the roles of lncRNAs in colon cancer liver metastasis are still largely unclear. In this study, we identified a novel lncRNA B3GALT5-AS1, which is reduced in colon cancer tissues and further reduced in colon cancer liver metastasis tissues. Reduced expression of B3GALT5-AS1 is associated with liver metastasis and poor outcome of colon cancer patients. Gain-of-function and loss-of-function assays revealed that B3GALT5-AS1 inhibited proliferation but promoted migration and invasion of colon cancer cells. Further investigation revealed that B3GALT5-AS1 directly bound to the promoter of miRNA-203, repressed miR-203 expression, upregulated miR-203 targets ZEB2 and SNAI2, and induced epithelial-to-mesenchymal transition (EMT). In vivo study revealed that B3GALT5-AS1 suppressed colon cancer liver metastasis via its binding on miR-203 promoter and the repression of miR-203. miR-203 is increased and epithelial phenotype is preferred in colon cancer liver metastasis tissues. Collectively, our data revealed the suppressive roles of B3GALT5-AS1/miR-203/EMT regulation axis in colon cancer liver metastasis. Our data suggested that the activating B3GALT5-AS1/miR-203/EMT axis may be potential therapeutic strategy for colon cancer liver metastasis.
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A functional variant of SMAD4 enhances macrophage recruitment and inflammatory response via TGF-β signal activation in Thoracic aortic aneurysm and dissection

Ying Wang, Pei Yin, Yi-Huan Chen, Yun-Sheng Yu, Wen-Xue Ye, Hao-Yue Huang, Zhen-Chun Ji, Zhen-Ya Shen,

https://doi.org/10.18632/aging.101662 pp 3683—3701

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Wang Y, Yin P, Chen Y, Yu Y, Ye W, Huang H, Ji Z, Shen Z, . A functional variant of SMAD4 enhances macrophage recruitment and inflammatory response via TGF-β signal activation in Thoracic aortic aneurysm and dissection. . 10:3683-3701. https://doi.org/10.18632/aging.101662

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 TY - JOUR
 AU - Wang, Ying 
 AU - Yin, Pei 
 AU - Chen, Yi-Huan 
 AU - Yu, Yun-Sheng 
 AU - Ye, Wen-Xue 
 AU - Huang, Hao-Yue 
 AU - Ji, Zhen-Chun 
 AU - Shen, Zhen-Ya 
 TI - A functional variant of SMAD4 enhances macrophage recruitment and inflammatory response via TGF-β signal activation in Thoracic aortic aneurysm and dissection
 JO - 
 JA - 
 VL - 10
 IS - 12
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101662
 DO - 10.18632/aging.101662
 SP - 3683
 EP - 3701
 PY - 
 AB - Thoracic aortic aneurysm and dissection (TAAD) is the most fatal macro vascular disease. The mortality of 48h after diagnosis of dissection is up to approximately 50-68%. However, the genetic factors and potential mechanism underlying sporadic TAAD remain largely unknown. Our previous study suggested rs12455792 variant of SMAD4 gene significantly contributed to the increased risk and might participated the pathological progression of TAAD. This investigation aims to test (1) the associations between rs12455792 and MØ recruitment, inflammatory response in aggressiveness of TAAD, and (2) the molecular mechanism accounting for their effects. In TGF-β signaling molecular detection, rs12455792 C&gt;T variant activated the canonical and non-canonical TGF-β mediators. It also increased the secretion of chemotactic factors of HASMCs. To confirm the impact of this change, we detected MØ recruitment and infiltration in HASMCs and aortic tissues of TAAD patients. We found that MØ recruitment in cells and tissues with rs12455792 variant genotypes was increased than that in wild type groups. Moreover, rs12455792 variant increased M1 type inflammatory response, which might contribute much to TAAD progression. To mimic the SMAD4 suppression effect of rs12455792 in vivo, we constructed the SMAD4 KD mouse. After induction with Ang II for 4w, the thoracic aorta dilatation and vascular remodeling were more serious than that of wild type group. In conclusion, rs12455792 increased MØ recruitment, M1 type inflammatory response via activated TGF-β signaling, and further promoted vascular remodeling and pathological progress of TAAD.
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BCAR4 activates GLI2 signaling in prostate cancer to contribute to castration resistance

Zhiping Cai, Yapei Wu, Yao Li, Jizhong Ren, Linhui Wang,

https://doi.org/10.18632/aging.101664 pp 3702—3712

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Cai Z, Wu Y, Li Y, Ren J, Wang L, . BCAR4 activates GLI2 signaling in prostate cancer to contribute to castration resistance. . 10:3702-3712. https://doi.org/10.18632/aging.101664

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                TY  - JOUR
                AU  - Cai, Zhiping 
                AU  - Wu, Yapei 
                AU  - Li, Yao 
                AU  - Ren, Jizhong 
                AU  - Wang, Linhui 
                TI  - BCAR4 activates GLI2 signaling in prostate cancer to contribute to castration resistance
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101664
                DO  - 10.18632/aging.101664
                SP  - 3702
                EP  - 3712
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) have been found essential for tumorigenesis of prostate cancer (PC), but its role in the regulation of castration-resistant prostate cancer (CRPC) is poorly identified. Here, we showed that a lncRNA, Breast-Cancer Anti-Estrogen Resistance 4 (BCAR4), which plays a pivotal role in the tamoxifen-resistance of breast cancer, was significantly upregulated in CRPC, but not in castration-sensitive prostate cancer (CSPC), compared to normal prostate tissue. High BCAR4 levels in CRPC were correlated with poor patients’ overall survival. Androgen increased growth and migration of androgen receptor (AR)-positive PC346 cells, which was abolished by the antagonist of androgen. Overexpression of BCAR4 in PC346 cells increased cell growth and migration, but turned the cells insensitive to androgen. On the other hand, growth and migration of AR-negative DU145 cells are insensitive to androgen, while depletion of BCAR4 in DU145 cells not only decreased cell growth, but also turned the cells sensitive again to androgen. Moreover, BCAR4 activated GLI2 downstream genes, and correlated with the levels of these GLI2-target genes in CRPC. Depletion of GLI2 abolished the effects of BCAR4 on cell growth and migration. Together, our data suggest that BCAR4 may activate GLI2 signaling in PC to contribute to castration resistance.
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Reduced production of laminin by hepatic stellate cells contributes to impairment in oval cell response to liver injury in aged mice

Liu Qian, Hui Zhang, Yuting Gu, Dechun Li, Songbing He, Hui Wang, Yiji Cheng, Wanlin Yang, Hongshuang Yu, Xiaonan Zhao, Wei Cai, Lijun Meng, Min Jin, Yanan Wang, Yanyun Zhang,

https://doi.org/10.18632/aging.101665 pp 3713—3735

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Qian L, Zhang H, Gu Y, Li D, He S, Wang H, Cheng Y, Yang W, Yu H, Zhao X, Cai W, Meng L, Jin M, et al, . Reduced production of laminin by hepatic stellate cells contributes to impairment in oval cell response to liver injury in aged mice. . 10:3713-3735. https://doi.org/10.18632/aging.101665

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                TY  - JOUR
                AU  - Qian, Liu 
                AU  - Zhang, Hui 
                AU  - Gu, Yuting 
                AU  - Li, Dechun 
                AU  - He, Songbing 
                AU  - Wang, Hui 
                AU  - Cheng, Yiji 
                AU  - Yang, Wanlin 
                AU  - Yu, Hongshuang 
                AU  - Zhao, Xiaonan 
                AU  - Cai, Wei 
                AU  - Meng, Lijun 
                AU  - Jin, Min 
                AU  - Wang, Yanan 
                AU  - Zhang, Yanyun 
                TI  - Reduced production of laminin by hepatic stellate cells contributes to impairment in oval cell response to liver injury in aged mice
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101665
                DO  - 10.18632/aging.101665
                SP  - 3713
                EP  - 3735
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Qian, Liu 
                AU  - Zhang, Hui 
                AU  - Gu, Yuting 
                AU  - Li, Dechun 
                AU  - He, Songbing 
                AU  - Wang, Hui 
                AU  - Cheng, Yiji 
                AU  - Yang, Wanlin 
                AU  - Yu, Hongshuang 
                AU  - Zhao, Xiaonan 
                AU  - Cai, Wei 
                AU  - Meng, Lijun 
                AU  - Jin, Min 
                AU  - Wang, Yanan 
                AU  - Zhang, Yanyun 
                TI  - Reduced production of laminin by hepatic stellate cells contributes to impairment in oval cell response to liver injury in aged mice
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101665
                DO  - 10.18632/aging.101665
                SP  - 3713
                EP  - 3735
                PY  - 
                AB  - Aged liver is usually impaired in response to hepatic injury. Tissue-specific stem cells participate in the repair of tissue injury. However, how oval cells (OCs) respond to injury and how the process is regulated by tissue microenvironment in aged mice have not been fully understood. In this study, taking advantage of well-established murine OC activation model, we demonstrated that OCs were less activated upon injury in aged mice and the impairment was mainly attributed to dysfunction in their niche. Through analyzing global gene expression, we found that the genes differentially expressed in damaged young and aged mouse liver tissues were predominantly those required for the formation and remodeling of extracellular matrix. As one of the most important extracellular matrix components in the OC niche, laminin was shown to promote the proliferation of OCs. Not surprisingly, laminin was downregulated with aging. Consistent with the downregulation of genes encoding DNA-dependent protein kinase (DNA-PK) proteins in aged hepatic stellate cells (HSCs), inhibition of DNA-PK also led to reduced expression of laminin in HSCs. Moreover, impairment in OC activation caused by less supporting from DNA-damaged HSCs could be rescued by laminin. This study reveals a new cellular mechanism underlying impaired OCs functionality during aging.
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Inhibition of protein kinase D disrupts spindle formation and actin assembly during porcine oocyte maturation

Yu Zhang, Hong-Hui Wang, Xiang Wan, Yao Xu, Meng-Hao Pan, Shao-Chen Sun,

https://doi.org/10.18632/aging.101667 pp 3736—3744

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Zhang Y, Wang H, Wan X, Xu Y, Pan M, Sun S, . Inhibition of protein kinase D disrupts spindle formation and actin assembly during porcine oocyte maturation. . 10:3736-3744. https://doi.org/10.18632/aging.101667

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                TY  - JOUR
                AU  - Zhang, Yu 
                AU  - Wang, Hong-Hui 
                AU  - Wan, Xiang 
                AU  - Xu, Yao 
                AU  - Pan, Meng-Hao 
                AU  - Sun, Shao-Chen 
                TI  - Inhibition of protein kinase D disrupts spindle formation and actin assembly during porcine oocyte maturation
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101667
                DO  - 10.18632/aging.101667
                SP  - 3736
                EP  - 3744
                PY  - 
                AB  - Protein kinase D (PKD) subfamily which includes PKD1, PKD2 and PKD3 is a novel family of serine/threonine kinases. PKD has been widely implicated in the regulation of multiple physiological effects including immune responses, apoptosis and cell proliferation. However, the roles of PKD in oocytes have not been fully clarified. In this study we investigated the regulatory functions of PKD during porcine oocyte maturation. Our results indicated that PKD expressed in porcine oocytes and the inhibition of PKD family activity led to the failure of meiosis resumption and the first polar body extrusion. Further analysis indicated that the spindle assembly and chromosome alignment were disrupted after PKD family inhibition, and this might be through its regulatory role on MAPK phosphorylation. We also found that PKD phosphorylated cofilin for actin assembly, which further affected cortical actin distribution, indicating the roles of PKD family on cytoskeleton. In addition, a decreased expression of PKD in postovulatory aging porcine oocytes was observed, which might connect PKD with cytoskeleton defects in aged oocytes. Taken together, these results suggest that PKD possesses important functions in porcine oocyte maturation by regulating spindle organization and actin assembly.
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TAp73 regulates ATP7A: possible implications for ageing-related diseases

Piervito Lopriore, Nazzareno Capitanio, Emanuele Panatta, Nicola Di Daniele, Alessandra Gambacurta, Gerry Melino, Ivano Amelio,

https://doi.org/10.18632/aging.101669 pp 3745—3760

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Lopriore P, Capitanio N, Panatta E, Di Daniele N, Gambacurta A, Melino G, Amelio I, . TAp73 regulates ATP7A: possible implications for ageing-related diseases. . 10:3745-3760. https://doi.org/10.18632/aging.101669

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                TY  - JOUR
                AU  - Lopriore, Piervito 
                AU  - Capitanio, Nazzareno 
                AU  - Panatta, Emanuele 
                AU  - Di Daniele, Nicola 
                AU  - Gambacurta, Alessandra 
                AU  - Melino, Gerry 
                AU  - Amelio, Ivano 
                TI  - TAp73 regulates ATP7A: possible implications for ageing-related diseases
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101669
                DO  - 10.18632/aging.101669
                SP  - 3745
                EP  - 3760
                PY  - 
                AB  - The p53 family member p73 controls a wide range of cellular function. Deletion of p73 in mice results in increased tumorigenesis, infertility, neurological defects and altered immune system. Despite the extensive effort directed to define the molecular underlying mechanism of p73 function a clear definition of its transcriptional signature and the extent of overlap with the other p53 family members is still missing. Here we describe a novel TAp73 target, ATP7A a member of a large family of P-type ATPases implicated in human neurogenerative conditions and cancer chemoresistance. Modulation of TAp73 expression influences basal expression level of ATP7A in different cellular models and chromatin immunoprecipitation confirmed a physical direct binding of TAp73 on ATP7A genomic regions. Bioinformatic analysis of expression profile datasets of human lung cancer patients suggests a possible implication of TAp73/ATP7A axis in human cancer. These data provide a novel TAp73-dependent target which might have implications in ageing-related diseases such as cancer and neurodegeneration.
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DNA methylation-based age prediction and telomere length in white blood cells and cumulus cells of infertile women with normal or poor response to ovarian stimulation

Scott J. Morin, Xin Tao, Diego Marin, Yiping Zhan, Jessica Landis, Jenna Bedard, Richard T. Scott Jr., Emre Seli,

https://doi.org/10.18632/aging.101670 pp 3761—3773

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Morin SJ, Tao X, Marin D, Zhan Y, Landis J, Bedard J, Scott RT, Seli E, . DNA methylation-based age prediction and telomere length in white blood cells and cumulus cells of infertile women with normal or poor response to ovarian stimulation. . 10:3761-3773. https://doi.org/10.18632/aging.101670

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                TY  - JOUR
                AU  - Morin, Scott J. 
                AU  - Tao, Xin 
                AU  - Marin, Diego 
                AU  - Zhan, Yiping 
                AU  - Landis, Jessica 
                AU  - Bedard, Jenna 
                AU  - Scott, Richard T. 
                AU  - Seli, Emre 
                TI  - DNA methylation-based age prediction and telomere length in white blood cells and cumulus cells of infertile women with normal or poor response to ovarian stimulation
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101670
                DO  - 10.18632/aging.101670
                SP  - 3761
                EP  - 3773
                PY  - 
                AB  - An algorithm assessing the methylation levels of 353 informative CpG sites in the human genome permits accurate prediction of the chronologic age of a subject. Interestingly, when there is discrepancy between the predicted age and chronologic age (age acceleration or “AgeAccel”), patients are at risk for morbidity and mortality. Identification of infertile patients at risk for accelerated reproductive senescence may permit preventative action. This study aimed to assess the accuracy of the “epigenetic clock” concept in reproductive age women undergoing fertility treatment by applying the age prediction algorithm in peripheral (white blood cells [WBCs]) and follicular somatic cells (cumulus cells [CCs]), and to identify whether women with premature reproductive aging (diminished ovarian reserve) were at risk of AgeAccel in their age prediction. Results indicated that the epigenetic algorithm accurately predicts age when applied to WBCs but not to CCs. The age prediction of CCs was substantially younger than chronologic age regardless of the patient’s age or response to stimulation. In addition, telomeres of CCs were significantly longer than that of WBCs. Our findings suggest that CCs do not demonstrate changes in methylome-predicted age or telomere-length in association with increasing female age or ovarian response to stimulation.
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A CREB1/miR-433 reciprocal feedback loop modulates proliferation and metastasis in colorectal cancer

Li Yan, Wei-Qiang You, Neng-Quan Sheng, Jian-Feng Gong, Lan-Dian Hu, Ge-Wen Tan, Hong-Qi Chen, Zhi-Gang Wang,

https://doi.org/10.18632/aging.101671 pp 3774—3793

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Yan L, You W, Sheng N, Gong J, Hu L, Tan G, Chen H, Wang Z, . A CREB1/miR-433 reciprocal feedback loop modulates proliferation and metastasis in colorectal cancer. . 10:3774-3793. https://doi.org/10.18632/aging.101671

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                TY  - JOUR
                AU  - Yan, Li 
                AU  - You, Wei-Qiang 
                AU  - Sheng, Neng-Quan 
                AU  - Gong, Jian-Feng 
                AU  - Hu, Lan-Dian 
                AU  - Tan, Ge-Wen 
                AU  - Chen, Hong-Qi 
                AU  - Wang, Zhi-Gang 
                TI  - A CREB1/miR-433 reciprocal feedback loop modulates proliferation and metastasis in colorectal cancer
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101671
                DO  - 10.18632/aging.101671
                SP  - 3774
                EP  - 3793
                PY  - 
                AB  - Increasing evidence has indicated the prognostic value of miR-433 across a series of malignancy types. However, the underlying mechanisms involved in cancer progression haven’t been sufficiently elucidated. In the present work, we found that miR-433 was downregulated in CRC tissues and cell lines. Ectopic expression of miR-433 obviously suppressed the proliferation, invasion and metastasis activity of CRC cells in vitro and in vivo. CREB1, CCAR1 and JNK1 were highly expressed and negatively correlated with miR-433 expression in CRC. CRC patients with higher expression of CREB1, CCAR1 or JNK1 presented a worse outcome relative to those with lower expression. CREB1 transactivated the expression of miR-433, and CREB1, CCAR1 and JNK1 simultaneously served as its targets, which in turn composed a feedback loop between CREB1 and miR-433. miR-433 blocked cell cycle progression and abolished EMT. Collectively, our study demonstrated the CREB1/miR-433 reciprocal feedback loop restrained the propagation, invasion and metastasis activities of CRC cells through abrogation of cell cycle progression and constraint of EMT.
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Sevoflurane impairs learning and memory of the developing brain through post-transcriptional inhibition of CCNA2 via microRNA-19-3p

Xin Zhao, Yanwu Jin, Haibo Li, Yuxiu Jia, Yuelan Wang,

https://doi.org/10.18632/aging.101673 pp 3794—3805

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Zhao X, Jin Y, Li H, Jia Y, Wang Y, . Sevoflurane impairs learning and memory of the developing brain through post-transcriptional inhibition of CCNA2 via microRNA-19-3p. . 10:3794-3805. https://doi.org/10.18632/aging.101673

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                TY  - JOUR
                AU  - Zhao, Xin 
                AU  - Jin, Yanwu 
                AU  - Li, Haibo 
                AU  - Jia, Yuxiu 
                AU  - Wang, Yuelan 
                TI  - Sevoflurane impairs learning and memory of the developing brain through post-transcriptional inhibition of CCNA2 via microRNA-19-3p
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101673
                DO  - 10.18632/aging.101673
                SP  - 3794
                EP  - 3805
                PY  - 
                AB  - The molecular mechanisms underlying sevoflurane (SEVO)-induced impairment of learning and memory remain unclear. Specifically, a role of microRNAs (miRNAs) in the control of the neuron proliferation in the developing brain exposed to SEVO has not been reported previously. Here, we studied the effects of SEVO exposure on the neural cell proliferation, and on the learning and memory of neonatal rats. We found that SEVO exposure significantly decreased neuron cell proliferation, reduced BDNF levels in brain, and impaired learning and memory of neonatal rats in Morris water maze test and Plus-Maze discriminative avoidance task (PM-DAT), likely through downregulation of CCNA2 protein. Next, we used bioinformatic tools to predict CCNA2-binding microRNAs (miRNAs), and found that miR-19-3p was upregulated in neurons exposed to SEVO. Moreover, miR-19-3p functionally inhibited the protein translation of CCNA2 in a human neural cell line, HCN-2. Furthermore, intracranial injection of adeno-associated virus carrying antisense of miR-19-3p under a CMV promoter into the neonatal rats significantly alleviated SEVO exposure-induced impairment of neuron cell proliferation, as well as the learning and memory of the rats. Together, our data suggest that SEVO-induced upregulation of miR-19-3p post-transcriptionally inhibits CCNA2, which contributes to the SEVO-associated impairment of learning and memory of the neonatal rats.
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Circular RNA EIF6 (Hsa_circ_0060060) sponges miR-144-3p to promote the cisplatin-resistance of human thyroid carcinoma cells by autophagy regulation

Feng Liu, Jin Zhang, Long Qin, Ziyao Yang, Jianxia Xiong, Yanyan Zhang, Ruihuan Li, Shujing Li, Huifang Wang, Bo Yu, Wenjun Zhao, Weiran Wang, Zhensu Li, Jing Liu,

https://doi.org/10.18632/aging.101674 pp 3806—3820

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Liu F, Zhang J, Qin L, Yang Z, Xiong J, Zhang Y, Li R, Li S, Wang H, Yu B, Zhao W, Wang W, Li Z, et al, . Circular RNA EIF6 (Hsa_circ_0060060) sponges miR-144-3p to promote the cisplatin-resistance of human thyroid carcinoma cells by autophagy regulation. . 10:3806-3820. https://doi.org/10.18632/aging.101674

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                TY  - JOUR
                AU  - Liu, Feng 
                AU  - Zhang, Jin 
                AU  - Qin, Long 
                AU  - Yang, Ziyao 
                AU  - Xiong, Jianxia 
                AU  - Zhang, Yanyan 
                AU  - Li, Ruihuan 
                AU  - Li, Shujing 
                AU  - Wang, Huifang 
                AU  - Yu, Bo 
                AU  - Zhao, Wenjun 
                AU  - Wang, Weiran 
                AU  - Li, Zhensu 
                AU  - Liu, Jing 
                TI  - Circular RNA EIF6 (Hsa_circ_0060060) sponges miR-144-3p to promote the cisplatin-resistance of human thyroid carcinoma cells by autophagy regulation
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101674
                DO  - 10.18632/aging.101674
                SP  - 3806
                EP  - 3820
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Liu, Feng 
                AU  - Zhang, Jin 
                AU  - Qin, Long 
                AU  - Yang, Ziyao 
                AU  - Xiong, Jianxia 
                AU  - Zhang, Yanyan 
                AU  - Li, Ruihuan 
                AU  - Li, Shujing 
                AU  - Wang, Huifang 
                AU  - Yu, Bo 
                AU  - Zhao, Wenjun 
                AU  - Wang, Weiran 
                AU  - Li, Zhensu 
                AU  - Liu, Jing 
                TI  - Circular RNA EIF6 (Hsa_circ_0060060) sponges miR-144-3p to promote the cisplatin-resistance of human thyroid carcinoma cells by autophagy regulation
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101674
                DO  - 10.18632/aging.101674
                SP  - 3806
                EP  - 3820
                PY  - 
                AB  - Anaplastic thyroid carcinoma (ATC) responds for the majority of death of thyroid carcinoma and often causes chemotherapy resistance. We investigated the influence of circEIF6 (Hsa_circ_0060060) on the cisplatin-sensitivity in papillary thyroid carcinoma (PTC) and ATC cells, and explored its regulation to downstream molecules miR-144-3p and Transforming Growth Factor α (TGF-α). Differentially expressed circRNAs in PTC were analyzed using the GSE93522 data downloaded. Expressions of circEIF6, miR-144-3p, TGF-α, autophagy-related proteins and apoptosis-related proteins were determined using qRT-PCR or western blot. RNA pull-down assay and dual luciferase report assay were applied to reveal the target relationships. Autophagy marker LC3 and cell proliferation marker ki67 were evaluated by immunofluorescence and immunohistochemistry. Cell viability was evaluated with MTT assay and cell apoptosis was assessed by flow cytometric analysis. CircEIF6, could promote autophagy induced by cisplatin, thus inhibiting cell apoptosis and enhancing the resistance of PTC and ATC cells to cisplatin. Has-miR-144-3p was the target of circEIF6 and was regulated by circEIF6. Besides, circEIF6 promoted autophagy by regulating miR-144-3p/TGF-α axis, enhancing the cisplatin-resistance in PTC and ATC cells. CircEIF6 promoted tumor growth by regulating miR-144-3p/TGF-α and circEIF6 knock-down enhanced cisplatin sensitivity in vivo. CircEIF6 could provide a target for therapy of cisplatin-resistance in thyroid carcinoma.
                ER  -

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Caloric restriction rescues yeast cells from alpha-synuclein toxicity through autophagic control of proteostasis

Belém Sampaio-Marques, Hélder Pereira, Ana R. Santos, Alexandra Teixeira, Paula Ludovico,

https://doi.org/10.18632/aging.101675 pp 3821—3833

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Sampaio-Marques B, Pereira H, Santos AR, Teixeira A, Ludovico P, . Caloric restriction rescues yeast cells from alpha-synuclein toxicity through autophagic control of proteostasis. . 10:3821-3833. https://doi.org/10.18632/aging.101675

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                TY  - JOUR
                AU  - Sampaio-Marques, Belém 
                AU  - Pereira, Hélder 
                AU  - Santos, Ana R. 
                AU  - Teixeira, Alexandra 
                AU  - Ludovico, Paula 
                TI  - Caloric restriction rescues yeast cells from alpha-synuclein toxicity through autophagic control of proteostasis
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101675
                DO  - 10.18632/aging.101675
                SP  - 3821
                EP  - 3833
                PY  - 
                AB  - α-Synuclein (SNCA) is a presynaptic protein that is associated with the pathophysiology of synucleinopathies, including Parkinson’s disease. SNCA is a naturally aggregation-prone protein, which may be degraded by the ubiquitin-proteasome system (UPS) and by lysosomal degradation pathways. Besides being a target of the proteolytic systems, SNCA can also alter the function of these pathways further, contributing to the progression of neurodegeneration. Deterioration of UPS and autophagy activities with aging further aggravates this toxic cycle. Caloric restriction (CR) is still the most effective non-genetic intervention promoting lifespan extension. It is known that CR-mediated lifespan extension is linked to the regulation of proteolytic systems, but the mechanisms underlying CR rescue of SNCA toxicity remain poorly understood. This study shows that CR balances UPS and autophagy activities during aging. CR enhances UPS activity, reversing the decline of the UPS activity promoted by SNCA, and keeps autophagy at homeostatic levels. Maintenance of autophagy at homeostatic levels appears to be relevant for UPS activity and for the mechanism underlying rescue of cells from SNCA-mediated toxicity by CR.
                ER  -

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Tissue iron is negatively correlated with TERC or TERT mRNA expression: a heterochronic parabiosis study in mice

Meng-Wan Zhang, Peng Zhao, Wing-Ho Yung, Yuan Sheng, Ya Ke, Zhong-Ming Qian,

https://doi.org/10.18632/aging.101676 pp 3834—3850

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Zhang M, Zhao P, Yung W, Sheng Y, Ke Y, Qian Z, . Tissue iron is negatively correlated with TERC or TERT mRNA expression: a heterochronic parabiosis study in mice. . 10:3834-3850. https://doi.org/10.18632/aging.101676

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                TY  - JOUR
                AU  - Zhang, Meng-Wan 
                AU  - Zhao, Peng 
                AU  - Yung, Wing-Ho 
                AU  - Sheng, Yuan 
                AU  - Ke, Ya 
                AU  - Qian, Zhong-Ming 
                TI  - Tissue iron is negatively correlated with TERC or TERT mRNA expression: a heterochronic parabiosis study in mice
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101676
                DO  - 10.18632/aging.101676
                SP  - 3834
                EP  - 3850
                PY  - 
                AB  - To test the hypothesis that iron accumulation in tissues with age is a key harmful factor for the development of aging, we established heterochronic parabiosis-pairings and investigated changes in serum iron, the expression of major iron transport proteins and iron contents, as well as telomerase reverse transcriptase (TERT), telomerase RNA component (TERC), and telomere length in the liver, kidney and heart of Y-O(O) (old pairing with young), Y-O(Y) (young pairing with old), O-O (pairings between two old) and Y-Y (pairings between two young) mice. We demonstrated that the reduced serum iron, increased iron and reduced expression of TERT and TERC in the tissues of aged mice are reversible by exposure to a younger mouse’s circulation. All of these measurements in young mice are reversible by exposure to an older mouse’s circulation. Correlation analysis showed that tissue iron is negatively correlated with TERT and TERC expression in the liver, kidney and heart of parabiotic mice. These findings provide new evidence for the key role of iron in aging and also imply the existence of rejuvenating factors in young serum with an anti-ageing role that act by reversing the impaired activity of iron metabolism in old mice.
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Aging-dependent decrease in the numbers of enteric neurons, interstitial cells of Cajal and expression of connexin43 in various regions of gastrointestinal tract

Tingyi Sun, Dandan Li, Shilong Hu, Li Huang, Haimei Sun, Shu Yang, Bo Wu, Fengqing Ji, Deshan Zhou,

https://doi.org/10.18632/aging.101677 pp 3851—3865

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Sun T, Li D, Hu S, Huang L, Sun H, Yang S, Wu B, Ji F, Zhou D, . Aging-dependent decrease in the numbers of enteric neurons, interstitial cells of Cajal and expression of connexin43 in various regions of gastrointestinal tract. . 10:3851-3865. https://doi.org/10.18632/aging.101677

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                TY  - JOUR
                AU  - Sun, Tingyi 
                AU  - Li, Dandan 
                AU  - Hu, Shilong 
                AU  - Huang, Li 
                AU  - Sun, Haimei 
                AU  - Yang, Shu 
                AU  - Wu, Bo 
                AU  - Ji, Fengqing 
                AU  - Zhou, Deshan 
                TI  - Aging-dependent decrease in the numbers of enteric neurons, interstitial cells of Cajal and expression of connexin43 in various regions of gastrointestinal tract
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101677
                DO  - 10.18632/aging.101677
                SP  - 3851
                EP  - 3865
                PY  - 
                AB  - Aging is a significant risk factor for gastrointestinal dysmotility, but aging-associated differences between different organs and the exact time to start degenerating have remained obscure. Here we evaluated alterations of interstitial cells of Cajal, enteric neurons and connexin43 expression in the stomach, jejunum and colon in 2-, 12-, 16-, 20- and 24-month-old mice, as well as in aged human colon. Interstitial cells of Cajal, cholinergic and nitrergic neurons within the whole digestive tract were reduced over time, but their loss first appeared in stomach, then in intestine, helping to understand that gastric function was first impaired during aging. The decrease of connexin43 expression occurred before interstitial cells of Cajal and neurons loss, suggesting that connexin43 might be the major target influenced during senescence. Furthermore, changes in expressions of pro-inflammatory cytokines (tumour necrosis factor-α, interleukin-1β, interleukin-6) and apoptosis-related proteins (B-cell lymphoma-2, caspase-3) which indicated “inflammaging”, might contribute to the loss of enteric neurons and interstitial cells of Cajal in aged gastrointestinal tract. Our results provide possible therapeutic time window for beneficial intervention for geriatric patients with gastrointestinal motility disorders.
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Serial position effects differ between Alzheimer’s and vascular features in mild cognitive impairment

Russell Jude Chander, Heidi Foo, Tingting Yong, Levinia Lim, Jayne Tan, Ming-Ching Wen, Adeline Ng, Shahul Hameed, Simon Ting, Juan Zhou, Nagaendran Kandiah,

https://doi.org/10.18632/aging.101678 pp 3866—3880

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Chander RJ, Foo H, Yong T, Lim L, Tan J, Wen M, Ng A, Hameed S, Ting S, Zhou J, Kandiah N, . Serial position effects differ between Alzheimer’s and vascular features in mild cognitive impairment. . 10:3866-3880. https://doi.org/10.18632/aging.101678

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                TY  - JOUR
                AU  - Chander, Russell Jude 
                AU  - Foo, Heidi 
                AU  - Yong, Tingting 
                AU  - Lim, Levinia 
                AU  - Tan, Jayne 
                AU  - Wen, Ming-Ching 
                AU  - Ng, Adeline 
                AU  - Hameed, Shahul 
                AU  - Ting, Simon 
                AU  - Zhou, Juan 
                AU  - Kandiah, Nagaendran 
                TI  - Serial position effects differ between Alzheimer’s and vascular features in mild cognitive impairment
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101678
                DO  - 10.18632/aging.101678
                SP  - 3866
                EP  - 3880
                PY  - 
                AB  - Individuals with mild cognitive impairment (MCI) exhibit varying serial position effect (SPE) performances. The relationship between SPE performance in word list recall and clinical, genetic, and neuroimaging features of MCI requires elucidation. 119 MCI and 68 cognitively normal (CN) participants underwent cognitive assessment, apolipoprotein E (ApoE) genotyping, and volumetric MRI brain scans processed via voxel-based morphometry. A 10-word recall task was used to assess SPE performance in relation to recency and primacy recall. MCI participants were classified as having Good SPE performance (high primacy and recency, Good SPE) or Poor SPE performance (low primacy only, LP-SPE; low recency only, LR-SPE; or both low, Low SPE). Poor SPE participants had reduced grey matter (GM) volumes and increased white matter hyperintensities (WMH) volumes. Participants with LP-SPE demonstrated reduced hippocampal GM volumes and were more likely to be ApoE ε4 carriers. LR-SPE was associated with higher WMH volumes. Presence of both greater WMH volumes and ApoE ε4 resulted in Low SPE. LP-SPE MCI participants had features typical of Alzheimer’s disease. LR-SPE MCI was associated with increased WMH volumes, likely representing vascular pathology. SPE profiles are associated with distinct clinical patterns of MCI pathophysiology and could have potential as a clinical marker.
                ER  -

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Accelerated aging induced by deficiency of Zmpste24 protects old mice to develop bleomycin-induced pulmonary fibrosis

Jazmín Calyeca, Yalbi I. Balderas-Martínez, Raúl Olmos, Rogelio Jasso, Vilma Maldonado, Quetzali Rivera, Moisés Selman, Annie Pardo,

https://doi.org/10.18632/aging.101679 pp 3881—3896

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Calyeca J, Balderas-Martínez YI, Olmos R, Jasso R, Maldonado V, Rivera Q, Selman M, Pardo A, . Accelerated aging induced by deficiency of Zmpste24 protects old mice to develop bleomycin-induced pulmonary fibrosis. . 10:3881-3896. https://doi.org/10.18632/aging.101679

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                TY  - JOUR
                AU  - Calyeca, Jazmín 
                AU  - Balderas-Martínez, Yalbi I. 
                AU  - Olmos, Raúl 
                AU  - Jasso, Rogelio 
                AU  - Maldonado, Vilma 
                AU  - Rivera, Quetzali 
                AU  - Selman, Moisés 
                AU  - Pardo, Annie 
                TI  - Accelerated aging induced by deficiency of Zmpste24 protects old mice to develop bleomycin-induced pulmonary fibrosis
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101679
                DO  - 10.18632/aging.101679
                SP  - 3881
                EP  - 3896
                PY  - 
                AB  - Idiopathic pulmonary fibrosis is a devastating aging-associated disease of unknown etiology. Despite that aging is a major risk factor, the mechanisms linking aging with this disease are uncertain, and experimental models to explore them in lung fibrosis are scanty. We examined the fibrotic response to bleomycin-induced lung injury in Zmpste24-deficient mice, which exhibit nuclear lamina defects developing accelerated aging. We found that young WT and Zmpste24(-/-) mice developed a similar fibrotic response to bleomycin. Unexpectedly, while old WT mice developed severe lung fibrosis, accelerated aged Zmpste24-/- mice were protected showing scant lung damage. To investigate possible mechanisms associated with this resistance to fibrosis, we compared the transcriptome signature of the lungs and found that Zmpste24(-/-) mice showed downregulation of several core and associated matrisome genes compared with WT mice. Interestingly, some microRNAs that target extracellular matrix molecules such as miR23a, miR27a, miR29a, miR29b-1, miR145a, and miR491 were dysregulated resulting in downregulation of profibrotic pathways such as TGF-β/SMAD3/NF-κB and Wnt3a/β-catenin signaling axis. These results indicate that the absence of Zmpste24 in aging mice results in impaired lung fibrotic response after injury, which is likely associated to the dysregulation of fibrosis-related miRNAs.
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Melatonin prevents deterioration in quality by preserving epigenetic modifications of porcine oocytes after prolonged culture

Junyu Nie, Peng Xiao, Xuefang Wang, Xiaogan Yang, Huiyan Xu, Kehuan Lu, Shengsheng Lu, Xingwei Liang,

https://doi.org/10.18632/aging.101680 pp 3897—3909

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Nie J, Xiao P, Wang X, Yang X, Xu H, Lu K, Lu S, Liang X, . Melatonin prevents deterioration in quality by preserving epigenetic modifications of porcine oocytes after prolonged culture. . 10:3897-3909. https://doi.org/10.18632/aging.101680

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                TY  - JOUR
                AU  - Nie, Junyu 
                AU  - Xiao, Peng 
                AU  - Wang, Xuefang 
                AU  - Yang, Xiaogan 
                AU  - Xu, Huiyan 
                AU  - Lu, Kehuan 
                AU  - Lu, Shengsheng 
                AU  - Liang, Xingwei 
                TI  - Melatonin prevents deterioration in quality by preserving epigenetic modifications of porcine oocytes after prolonged culture
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101680
                DO  - 10.18632/aging.101680
                SP  - 3897
                EP  - 3909
                PY  - 
                AB  - Prolonged culture of metaphase II oocytes is an in vitro aging process that compromises oocyte quality. We tested whether melatonin preserves epigenetic modifications in oocytes after prolonged culture. The porcine oocytes were maturated in vitro for 44 h, and then metaphase II oocytes were continuously cultured in medium supplemented with or without melatonin for 24 h. We found that the parthenogenetic blastocyst formation rate of prolonged-culture oocytes was lower than in fresh oocytes. We further observed that methylation at H3K4me2 and H3K27me2 of oocytes enhanced after prolonged culture. However, 5mc fluorescence intensity was lower in prolonged-culture oocytes than in fresh oocytes. Moreover, the promoter of the imprinted gene NNAT exhibited a higher level of DNA methylation in prolonged-culture oocytes than in fresh oocytes, which was associated with a reduced expression level and glucose uptake capability. Conversely, melatonin improved blastocyst formation rate and preserved histone and DNA methylation modifications, as well as NNAT function in the oocytes after prolonged culture. Notably, DNA methyltransferase inhibitor 5-aza significantly attenuated the protective role of melatonin on genomic DNA methylation. In summary, our results revealed that epigenetic modifications are disrupted in oocytes after prolonged culture, but the changes are reversed by melatonin.
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SIN-3 as a key determinant of lifespan and its sex dependent differential role on healthspan in Caenorhabditis elegans

Renu Pandey, Meenakshi Sharma, Daman Saluja,

https://doi.org/10.18632/aging.101682 pp 3910—3937

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Pandey R, Sharma M, Saluja D, . SIN-3 as a key determinant of lifespan and its sex dependent differential role on healthspan in Caenorhabditis elegans. . 10:3910-3937. https://doi.org/10.18632/aging.101682

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Provider: 
 TY - JOUR
 AU - Pandey, Renu 
 AU - Sharma, Meenakshi 
 AU - Saluja, Daman 
 TI - SIN-3 as a key determinant of lifespan and its sex dependent differential role on healthspan in Caenorhabditis elegans
 JO - 
 JA - 
 VL - 10
 IS - 12
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101682
 DO - 10.18632/aging.101682
 SP - 3910
 EP - 3937
 PY - 
 AB - Aging/senescence includes not just decline in lifespan but also etiologies of age associated morbidities which are inadequately understood. Extensive research has been undertaken to delineate the pathways and generate mutants with extended lifespan. However, little is known about the health status of these long lived mutants in the background of important genetic perturbations. Caenorhabditis elegans is one of the leading in vivo model organisms to study aging. Deletion of SIN-3, a transcription coregulator in C. elegans has been shown to reduce the lifespan of the mutant worms by half as compared to the wild-type and isogenic controls. The current study focuses on the effect of SIN-3 deletion on the healthspan of the worms. We find that not only are sin-3 mutants more susceptible to stress, but the overall stress intolerance and physiological decline is sex dependent. The severity of the phenotype is more pronounced in hermaphrodites as compared to the males carrying the same mutation with respect to the controls. The results further suggest that genetic perturbation along with the gender play an important role in determining the lifespan, healthspan and overall fitness of an organism.
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Higher gene expression stability during aging in long-lived giant mole-rats than in short-lived rats

Arne Sahm, Martin Bens, Yoshiyuki Henning, Christiane Vole, Marco Groth, Matthias Schwab, Steve Hoffmann, Matthias Platzer, Karol Szafranski, Philip Dammann,

https://doi.org/10.18632/aging.101683 pp 3938—3956

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Sahm A, Bens M, Henning Y, Vole C, Groth M, Schwab M, Hoffmann S, Platzer M, Szafranski K, Dammann P, . Higher gene expression stability during aging in long-lived giant mole-rats than in short-lived rats. . 10:3938-3956. https://doi.org/10.18632/aging.101683

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                TY  - JOUR
                AU  - Sahm, Arne 
                AU  - Bens, Martin 
                AU  - Henning, Yoshiyuki 
                AU  - Vole, Christiane 
                AU  - Groth, Marco 
                AU  - Schwab, Matthias 
                AU  - Hoffmann, Steve 
                AU  - Platzer, Matthias 
                AU  - Szafranski, Karol 
                AU  - Dammann, Philip 
                TI  - Higher gene expression stability during aging in long-lived giant mole-rats than in short-lived rats
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101683
                DO  - 10.18632/aging.101683
                SP  - 3938
                EP  - 3956
                PY  - 
                AB  - Many aging-associated physiological changes are known to occur in short- and long-lived species with different trajectories. Emerging evidence suggests that numerous life history trait differences between species are based on interspecies variations in gene expression. Little information is available, however, about differences in transcriptome changes during aging between mammals with diverging lifespans. For this reason, we studied the transcriptomes of five tissue types and two age cohorts of two similarly sized rodent species with very different lifespans: laboratory rats (Rattus norvegicus) and giant mole-rats (Fukomys mechowii), with maximum lifespans of 3.8 and more than 20 years, respectively. Our findings show that giant mole-rats exhibit higher gene expression stability during aging than rats. Although well-known aging signatures were detected in all tissue types of rats, they were found in only one tissue type of giant mole-rats. Furthermore, many differentially expressed genes that were found in both species were regulated in opposite directions during aging. This suggests that expression changes which cause aging in short-lived species are counteracted in long-lived species. Taken together, we conclude that expression stability in giant mole rats (and potentially in African mole-rats in general) may be one key factor for their long and healthy life.
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Integrated multi-omics characterization reveals a distinctive metabolic signature and the role of NDUFA4L2 in promoting angiogenesis, chemoresistance, and mitochondrial dysfunction in clear cell renal cell carcinoma

Giuseppe Lucarelli, Monica Rutigliano, Fabio Sallustio, Domenico Ribatti, Andrea Giglio, Martina Lepore Signorile, Valentina Grossi, Paola Sanese, Anna Napoli, Eugenio Maiorano, Cristina Bianchi, Roberto A. Perego, Matteo Ferro, Elena Ranieri, Grazia Serino, Lauren N. Bell, Pasquale Ditonno, Cristiano Simone, Michele Battaglia,

https://doi.org/10.18632/aging.101685 pp 3957—3985

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Lucarelli G, Rutigliano M, Sallustio F, Ribatti D, Giglio A, Lepore Signorile M, Grossi V, Sanese P, Napoli A, Maiorano E, Bianchi C, Perego RA, Ferro M, et al, . Integrated multi-omics characterization reveals a distinctive metabolic signature and the role of NDUFA4L2 in promoting angiogenesis, chemoresistance, and mitochondrial dysfunction in clear cell renal cell carcinoma. . 10:3957-3985. https://doi.org/10.18632/aging.101685

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                TY  - JOUR
                AU  - Lucarelli, Giuseppe 
                AU  - Rutigliano, Monica 
                AU  - Sallustio, Fabio 
                AU  - Ribatti, Domenico 
                AU  - Giglio, Andrea 
                AU  - Lepore Signorile, Martina 
                AU  - Grossi, Valentina 
                AU  - Sanese, Paola 
                AU  - Napoli, Anna 
                AU  - Maiorano, Eugenio 
                AU  - Bianchi, Cristina 
                AU  - Perego, Roberto A. 
                AU  - Ferro, Matteo 
                AU  - Ranieri, Elena 
                AU  - Serino, Grazia 
                AU  - Bell, Lauren N. 
                AU  - Ditonno, Pasquale 
                AU  - Simone, Cristiano 
                AU  - Battaglia, Michele 
                TI  - Integrated multi-omics characterization reveals a distinctive metabolic signature and the role of NDUFA4L2 in promoting angiogenesis, chemoresistance, and mitochondrial dysfunction in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101685
                DO  - 10.18632/aging.101685
                SP  - 3957
                EP  - 3985
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lucarelli, Giuseppe 
                AU  - Rutigliano, Monica 
                AU  - Sallustio, Fabio 
                AU  - Ribatti, Domenico 
                AU  - Giglio, Andrea 
                AU  - Lepore Signorile, Martina 
                AU  - Grossi, Valentina 
                AU  - Sanese, Paola 
                AU  - Napoli, Anna 
                AU  - Maiorano, Eugenio 
                AU  - Bianchi, Cristina 
                AU  - Perego, Roberto A. 
                AU  - Ferro, Matteo 
                AU  - Ranieri, Elena 
                AU  - Serino, Grazia 
                AU  - Bell, Lauren N. 
                AU  - Ditonno, Pasquale 
                AU  - Simone, Cristiano 
                AU  - Battaglia, Michele 
                TI  - Integrated multi-omics characterization reveals a distinctive metabolic signature and the role of NDUFA4L2 in promoting angiogenesis, chemoresistance, and mitochondrial dysfunction in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101685
                DO  - 10.18632/aging.101685
                SP  - 3957
                EP  - 3985
                PY  - 
                AB  - An altered metabolism is involved in the development of clear cell - renal cell carcinoma (ccRCC), and in this tumor many altered genes play a fundamental role in controlling cell metabolic activities. We delineated a large-scale metabolomic profile of human ccRCC, and integrated it with transcriptomic data to connect the variations in cancer metabolism with gene expression changes. Moreover, to better analyze the specific contribution of metabolic gene alterations potentially associated with tumorigenesis and tumor progression, we evaluated the transcription profile of primary renal tumor cells. Untargeted metabolomic analysis revealed a signature of an increased glucose uptake and utilization in ccRCC. In addition, metabolites related to pentose phosphate pathway were also altered in the tumor samples in association with changes in Krebs cycle intermediates and related metabolites. We identified NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 4-like 2 (NDUFA4L2) as the most highly expressed gene in renal cancer cells and evaluated its role in sustaining angiogenesis, chemoresistance, and mitochondrial dysfunction. Finally, we showed that silencing of NDUFA4L2 affects cell viability, increases mitochondrial mass, and induces ROS generation in hypoxia.
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Injury factors alter miRNAs profiles of exosomes derived from islets and circulation

Qi Fu, Hemin Jiang, Zibin Wang, Xingyun Wang, Heng Chen, Ziyang Shen, Lei Xiao, Xirong Guo, Tao Yang,

https://doi.org/10.18632/aging.101689 pp 3986—3999

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Fu Q, Jiang H, Wang Z, Wang X, Chen H, Shen Z, Xiao L, Guo X, Yang T, . Injury factors alter miRNAs profiles of exosomes derived from islets and circulation. . 10:3986-3999. https://doi.org/10.18632/aging.101689

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                TY  - JOUR
                AU  - Fu, Qi 
                AU  - Jiang, Hemin 
                AU  - Wang, Zibin 
                AU  - Wang, Xingyun 
                AU  - Chen, Heng 
                AU  - Shen, Ziyang 
                AU  - Xiao, Lei 
                AU  - Guo, Xirong 
                AU  - Yang, Tao 
                TI  - Injury factors alter miRNAs profiles of exosomes derived from islets and circulation
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101689
                DO  - 10.18632/aging.101689
                SP  - 3986
                EP  - 3999
                PY  - 
                AB  - Islets damage is a major abnormality underling diabetes. Recent studies suggested the value of exosomes in diagnosis. This study aimed to investigate the impact of injury factors on the miRNA profiles of islet exosomes and determine whether circulating exosomal miRNAs is suitable as biomarkers of islets damage. Islets were isolated from ICR mice and induced injury in vitro by mixed cytokines (Tumor Necrosis Factor-α, Interleukin -1β and Interferon-γ) or streptozotocin (STZ), and exosomes were derived from the cultural supernatant. Using miRNA microarray analysis, we found 22 and 11 differentially expressed miRNAs in islet exosomes of STZ and cytokines treatment, respectively, including 6 miRNAs as the intersection of two injured conditions. Thereinto, mmu-miR-375-3p and mmu-miR-129-5p could be validated by qRT-PCR. Then, Serum exosomes were isolated from STZ injected mice and subjects with various glucose metabolism states and diabetic duration. qRT-PCR demonstrated exosomal mmu-miR-375-3p dramatically increased in serum of STZ treated mouse prior to the disturbance of blood glucose and insulin. In human serum exosomes, hsa-miR-375-3p was elevated in new-onset diabetes patients. Overall, our results suggest that injury factors changed miRNA profiles of exosomes derived from islets and exosomal miR-375-3p showed promising potential as a biomarker of islets damage.
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The ER-alpha mutation Y537S confers Tamoxifen-resistance via enhanced mitochondrial metabolism, glycolysis and Rho-GDI/PTEN signaling: Implicating TIGAR in somatic resistance to endocrine therapy

Marco Fiorillo, Rosa Sanchez-Alvarez, Federica Sotgia, Michael P. Lisanti,

https://doi.org/10.18632/aging.101690 pp 4000—4023

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Fiorillo M, Sanchez-Alvarez R, Sotgia F, Lisanti MP, . The ER-alpha mutation Y537S confers Tamoxifen-resistance via enhanced mitochondrial metabolism, glycolysis and Rho-GDI/PTEN signaling: Implicating TIGAR in somatic resistance to endocrine therapy. . 10:4000-4023. https://doi.org/10.18632/aging.101690

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                TY  - JOUR
                AU  - Fiorillo, Marco 
                AU  - Sanchez-Alvarez, Rosa 
                AU  - Sotgia, Federica 
                AU  - Lisanti, Michael P. 
                TI  - The ER-alpha mutation Y537S confers Tamoxifen-resistance via enhanced mitochondrial metabolism, glycolysis and Rho-GDI/PTEN signaling: Implicating TIGAR in somatic resistance to endocrine therapy
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101690
                DO  - 10.18632/aging.101690
                SP  - 4000
                EP  - 4023
                PY  - 
                AB  - Naturally-occurring somatic mutations in the estrogen receptor gene (ESR1) have been previously implicated in the clinical development of resistance to hormonal therapies, such as Tamoxifen. For example, the somatic mutation Y537S has been specifically associated with acquired endocrine resistance. Briefly, we recombinantly-transduced MCF7 cells with a lentiviral vector encoding ESR1 (Y537S). As a first step, we confirmed that MCF7-Y537S cells are indeed functionally resistant to Tamoxifen, as compared with vector alone controls. Importantly, further phenotypic characterization of Y537S cells revealed that they show increased resistance to Tamoxifen-induced apoptosis, allowing them to form mammospheres with higher efficiency, in the presence of Tamoxifen. Similarly, Y537S cells had elevated basal levels of ALDH activity, a marker of “stemness”, which was also Tamoxifen-resistant. Metabolic flux analysis of Y537S cells revealed a hyper-metabolic phenotype, with significantly increased mitochondrial respiration and high ATP production, as well as enhanced aerobic glycolysis. Finally, to understand which molecular signaling pathways that may be hyper-activated in Y537S cells, we performed unbiased label-free proteomics analysis. Our results indicate that TIGAR over-expression and the Rho-GDI/PTEN signaling pathway appear to be selectively activated by the Y537S mutation. Remarkably, this profile is nearly identical in MCF7-TAMR cells; these cells were independently-generated in vitro, suggesting a highly conserved mechanism underlying Tamoxifen-resistance. Importantly, we show that the Y537S mutation is specifically associated with the over-expression of a number of protein markers of poor clinical outcome (COL6A3, ERBB2, STAT3, AFP, TFF1, CDK4 and CD44). In summary, we have uncovered a novel metabolic mechanism leading to endocrine resistance, which may have important clinical implications for improving patient outcomes.
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SNCA overexpression disturbs hippocampal gene expression trajectories in midlife

Thomas Hentrich, Zinah Wassouf, Olaf Riess, Julia M. Schulze-Hentrich,

https://doi.org/10.18632/aging.101691 pp 4024—4041

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Hentrich T, Wassouf Z, Riess O, Schulze-Hentrich JM, . SNCA overexpression disturbs hippocampal gene expression trajectories in midlife. . 10:4024-4041. https://doi.org/10.18632/aging.101691

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 TY - JOUR
 AU - Hentrich, Thomas 
 AU - Wassouf, Zinah 
 AU - Riess, Olaf 
 AU - Schulze-Hentrich, Julia M. 
 TI - SNCA overexpression disturbs hippocampal gene expression trajectories in midlife
 JO - 
 JA - 
 VL - 10
 IS - 12
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101691
 DO - 10.18632/aging.101691
 SP - 4024
 EP - 4041
 PY - 
 AB - Synucleinopathies like Parkinson’s disease and dementia with Lewy bodies originate from a complex and still largely enigmatic interplay of genetic predisposition, age, and environmental factors. While progressively declining motor functions hallmark late-life symptoms, first signs of the disease often surface already decades earlier during midlife. To better understand early disease stages with respect to the genetic, temporal, and environmental dimension, we interrogated hippocampal transcriptome data obtained during midlife for a mouse model overexpressing human SNCA, a pivotal gene in synucleinopathies, under different environments. To relate differentially expressed genes to human, we integrated expression signatures for aging and Parkinson’s disease. We identified two distinctive modes of age-dependent disturbances: First, cellular processes seemingly activated too early that reflected advanced stages of age and, second, typical longitudinal adaptations of the system that no longer occurred during midlife. Environmental enrichment prevented both disturbances modes despite persistent SNCA overload. Together, our results caution the view that expression changes characterising early stages of SNCA-related pathology reflect accelerated aging alone. Instead, we provide evidence that failure to undergo healthy adaptions during midlife represents a second origin of disturbances. This bimodal disturbance principle could inform therapeutic efforts to distinguish between preventive and restorative attempts to target the disease.
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Assessing onset, prevalence and survival in mice using a frailty phenotype

Cory W. Baumann, Dongmin Kwak, LaDora V. Thompson,

https://doi.org/10.18632/aging.101692 pp 4042—4053

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Baumann CW, Kwak D, Thompson LV, . Assessing onset, prevalence and survival in mice using a frailty phenotype. . 10:4042-4053. https://doi.org/10.18632/aging.101692

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                TY  - JOUR
                AU  - Baumann, Cory W. 
                AU  - Kwak, Dongmin 
                AU  - Thompson, LaDora V. 
                TI  - Assessing onset, prevalence and survival in mice using a frailty phenotype
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101692
                DO  - 10.18632/aging.101692
                SP  - 4042
                EP  - 4053
                PY  - 
                AB  - Little is known whether frailty assessments in mice are capable of distinguishing important characteristics of the frailty syndrome. The goals of this study were to identify the onset and the prevalence of frailty across the lifespan and to determine if a frailty phenotype predicts mortality. Body weight, walking speed, strength, endurance and physical activity were assessed in male C57BL/6 mice every three months starting at 14 months of age. Mice that fell in the bottom 20% for walking speed, strength, endurance and physical activity, and in the top 20% for body weight were considered to have a positive frailty marker. The onset of frailty occurred at 17 months, and represented only 3.5% of the mouse cohort. The percentage of frail mice increased with age until basically every mouse was identified as frail. Frail, pre-frail, and non-frail mice had mean survival ages of 27, 29 and 34 months, respectively. In closing, frail mice lack resilience; in that, multiple tissue/organ systems may deteriorate at an accelerated rate and ultimately lead to early mortality when compared to non-frail mice. Identifying the onset and prevalence of frailty, in addition to predicting mortality, has potential to yield information about several aging processes.
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Association of gut microbiota composition and function with a senescence-accelerated mouse model of Alzheimer’s Disease using 16S rRNA gene and metagenomic sequencing analysis

Weijun Peng, Pengji Yi, Jingjing Yang, Panpan Xu, Yang Wang, Zheyu Zhang, Siqi Huang, Zhe Wang, Chunhu Zhang,

https://doi.org/10.18632/aging.101693 pp 4054—4065

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Peng W, Yi P, Yang J, Xu P, Wang Y, Zhang Z, Huang S, Wang Z, Zhang C, . Association of gut microbiota composition and function with a senescence-accelerated mouse model of Alzheimer’s Disease using 16S rRNA gene and metagenomic sequencing analysis. . 10:4054-4065. https://doi.org/10.18632/aging.101693

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                TY  - JOUR
                AU  - Peng, Weijun 
                AU  - Yi, Pengji 
                AU  - Yang, Jingjing 
                AU  - Xu, Panpan 
                AU  - Wang, Yang 
                AU  - Zhang, Zheyu 
                AU  - Huang, Siqi 
                AU  - Wang, Zhe 
                AU  - Zhang, Chunhu 
                TI  - Association of gut microbiota composition and function with a senescence-accelerated mouse model of Alzheimer’s Disease using 16S rRNA gene and metagenomic sequencing analysis
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101693
                DO  - 10.18632/aging.101693
                SP  - 4054
                EP  - 4065
                PY  - 
                AB  - Although an intriguing potential association of the gut microbiome with Alzheimer's disease (AD) has attracted recent interest, few studies have directly assessed this relationship or underlying mechanism. Here, we compared the gut microbiota composition and functional differentiation of senescence-accelerated mouse prone 8 (SAMP8) mice with control senescence-accelerated mouse resistant 1 (SAMR1) mice using 16S rRNA gene and metagenomic sequencing analysis, respectively. Specifically, 16S sequencing results showed that the SAMP8 mice displayed a characteristic composition of the gut microbiome that clearly differed from that of the SAMR1 mice. Moreover, network analysis revealed that the gut microbiota of SAMP8 mice had decreased correlation density and clustering of operational taxonomic units. Metagenomic results revealed that the predominant Cluster of Orthologous Groups functional category related to these changes was the metabolism cluster in SAMP8 mice. The Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation further demonstrated enrichment of the relative abundance of some dominant metabolism-related KEGG pathways in the SAMP8 mice, consistent with the suggested pathogenic mechanisms of AD. In conclusion, this study suggests that perturbations of the gut microbiota composition and the functional metagenome may be associated with AD. Further studies are warranted to elucidate the potential new mechanism contributing to AD progression.
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Diminished circulating retinol and elevated α-TOH/retinol ratio predict an increased risk of cognitive decline in aging Chinese adults, especially in subjects with ApoE2 or ApoE4 genotype

Xiaochen Huang, Huiqiang Zhang, Jie Zhen, Shengqi Dong, Yujie Guo, Nicholas Van Halm-Lutterodt, Linhong Yuan,

https://doi.org/10.18632/aging.101694 pp 4066—4083

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Huang X, Zhang H, Zhen J, Dong S, Guo Y, Van Halm-Lutterodt N, Yuan L, . Diminished circulating retinol and elevated α-TOH/retinol ratio predict an increased risk of cognitive decline in aging Chinese adults, especially in subjects with ApoE2 or ApoE4 genotype. . 10:4066-4083. https://doi.org/10.18632/aging.101694

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                TY  - JOUR
                AU  - Huang, Xiaochen 
                AU  - Zhang, Huiqiang 
                AU  - Zhen, Jie 
                AU  - Dong, Shengqi 
                AU  - Guo, Yujie 
                AU  - Van Halm-Lutterodt, Nicholas 
                AU  - Yuan, Linhong 
                TI  - Diminished circulating retinol and elevated α-TOH/retinol ratio predict an increased risk of cognitive decline in aging Chinese adults, especially in subjects with ApoE2 or ApoE4 genotype
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101694
                DO  - 10.18632/aging.101694
                SP  - 4066
                EP  - 4083
                PY  - 
                AB  - Objective: The current study evaluated the relationship between circulating fat soluble vitamin status and cognition in aging Chinese population.Methods: A cross-sectional study was carried out in 1754 community residents aged 55-80 years aiming to evaluate the relationship between circulating α-tocopherol and retinol status and cognition. The effect of ApoE genetic polymorphism on the relationship between vitamins and cognition was also explored.Results: Our results indicated that serum retinol status positively correlated with cognitive performance; while, serum α-tocopherol (α-TOH)/retinol ratio negatively correlated with cognitive performance. Mild cognitive impairment (MCI) subject demonstrated higher serum α-TOH status (P &lt; 0.05), α-TOH/retinol ratio (P &lt; 0.01) and lower retinol status (P &lt; 0.01) than normal subjects. Subjects with ApoE4 genotype have lower serum retinol level (P &lt; 0.05) and higher α-TOH/retinol ratio (P &lt; 0.01) than subjects with ApoE3 genotype. MCI-ApoE4 carriers demonstrated the worst cognitive performance (P &lt; 0.05) and exhibited higher serum TC, α-TOH and α-TOH/retinol ratio levels (P &lt; 0.05), and lower LDL-C, retinol and lipid-adjusted retinol status (P &lt; 0.05). MCI-ApoE2 subjects showed higher serum TC, HDL-C content and α-TOH/retinol ratio (P &lt; 0.05); and lower serum retinol and lipid-adjusted retinol status (P &lt; 0.05).Conclusion: Lower circulating retinol and higher α-TOH/retinol ratio potentially predicts an increased risk for the development of cognitive decline in aging Chinese adults. ApoE2 or E4 carriers with higher circulating α-TOH/retinol ratio infer poor cognitive performance and an increased risk of developing MCI.
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Two variants of Interleukin-1B gene are associated with the decreased risk, clinical features, and better overall survival of colorectal cancer: a two-center case-control study

Haihua Qian, Dan Zhang, Chuanqing Bao,

https://doi.org/10.18632/aging.101695 pp 4084—4092

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Qian H, Zhang D, Bao C, . Two variants of Interleukin-1B gene are associated with the decreased risk, clinical features, and better overall survival of colorectal cancer: a two-center case-control study. . 10:4084-4092. https://doi.org/10.18632/aging.101695

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                TY  - JOUR
                AU  - Qian, Haihua 
                AU  - Zhang, Dan 
                AU  - Bao, Chuanqing 
                TI  - Two variants of Interleukin-1B gene are associated with the decreased risk, clinical features, and better overall survival of colorectal cancer: a two-center case-control study
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101695
                DO  - 10.18632/aging.101695
                SP  - 4084
                EP  - 4092
                PY  - 
                AB  - Interleukin (IL)-1B reportedly promotes the stemness and invasiveness of colon cancer cells. Several studies have investigated the association between IL-1B gene polymorphisms and colorectal cancer (CRC) risk, but report conflicting findings. Here, this association was explored in a hospital-based case-control study involving 527 CRC cases and 639 controls from two Chinese Han populations. Genotyping was done by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The IL-1B expression in CRC patients and controls were obtained from the GEPIA database and the mRNA expressions of different genotypes were downloaded from the GTEx portal database. The relationship of two IL-1B gene loci with clinical parameters and overall survival were analyzed using the Chi-square test and Kaplan-Meier analysis with the log-rank test respectively. It was found that the IL-1B mRNA levels in CRC patients were significantly higher than in controls. Bioinformatic analysis suggested that rs1143634 and rs1143623 polymorphisms decreased the IL-1B mRNA expression. The two polymorphisms were associated with decreased risk for CRC. Stratified analyses revealed the IL-1B gene rs1143623 and rs1143634 polymorphisms decreased the risk of CRC among females, smokers and drinkers. Moreover, the CC and/or GC genotype of rs1143623 polymorphism were correlated with decreased risk among CRC patients with tumor size ≥5cm, TNM stage III+IV, and rectal cancer. For rs1143634 polymorphism, the CT genotype reduced the risk of colorectal adenocarcinoma. The CRC patients carrying CC genotype of rs1143623 polymorphism were associated with better overall survival. In conclusion, IL-1B gene rs1143623 and rs1143634 polymorphisms are associated with decreased risk for CRC patients and thereby play important roles in the etiology of CRC.
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Putrescine delays postovulatory aging of mouse oocytes by upregulating PDK4 expression and improving mitochondrial activity

Wendan Xu, Lingjun Li, Jingwen Sun, Songyue Zhu, Zhengjie Yan, Li Gao, Chao Gao, Yugui Cui, Caiping Mao,

https://doi.org/10.18632/aging.101699 pp 4093—4106

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Xu W, Li L, Sun J, Zhu S, Yan Z, Gao L, Gao C, Cui Y, Mao C, . Putrescine delays postovulatory aging of mouse oocytes by upregulating PDK4 expression and improving mitochondrial activity. . 10:4093-4106. https://doi.org/10.18632/aging.101699

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                TY  - JOUR
                AU  - Xu, Wendan 
                AU  - Li, Lingjun 
                AU  - Sun, Jingwen 
                AU  - Zhu, Songyue 
                AU  - Yan, Zhengjie 
                AU  - Gao, Li 
                AU  - Gao, Chao 
                AU  - Cui, Yugui 
                AU  - Mao, Caiping 
                TI  - Putrescine delays postovulatory aging of mouse oocytes by upregulating PDK4 expression and improving mitochondrial activity
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101699
                DO  - 10.18632/aging.101699
                SP  - 4093
                EP  - 4106
                PY  - 
                AB  - If fertilization does not occur for a prolonged period in vivo or in vitro, the postovulatory oocytes will deteriorate, which called the postovulatory aging. This process disrupts the developmental competence. In the present study, we showed that the reactive oxygen species (ROS) was accumulated in oocytes during the postovulatory aging. ROS inhibited Sirt1 expression, and then increased oxidative stress by downregulating the intracellular Sirt1-FOXO3a-SOD2 axis. Moreover, the inhibited Sirt1 expression was related to the decreased mitochondrial function and the lowered level of autophagy. The mitochondrial-related apoptosis was increased by inhibiting the AKT and ERK1/2 pathways, due to the accumulation of ROS in the postovulatory oocytes. The mitochondrial pyruvate dehydrogenase kinase-4 (PDK4) can reduce ROS by inhibiting the tricarboxylic acid (TAC) cycle. We found that PDK4 was significantly decreased in the postovulatory aging oocytes. Putrescine, one of the abundant biogenic amines, ameliorated the effects of ROS and therefore improved the quality of the postovulatory aging oocytes by increasing the expression of PDK4. When PDK4 was downregulated using siRNAs, the effects of putrescine were significantly receded. We concluded that putrescine delayed the aging process of postovulatory oocytes by upregulating PDK4 expression and improving mitochondrial activity.
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Comparisons of metastatic patterns of colorectal cancer among patients by age group: a population-based study

Lin Yang, Xingli Yang, Wenzhuo He, Shousheng Liu, Chang Jiang, Kunqian Xie, Kunwei Peng, Yafei You, Bei Zhang, Liangping Xia,

https://doi.org/10.18632/aging.101700 pp 4107—4119

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Yang L, Yang X, He W, Liu S, Jiang C, Xie K, Peng K, You Y, Zhang B, Xia L, . Comparisons of metastatic patterns of colorectal cancer among patients by age group: a population-based study. . 10:4107-4119. https://doi.org/10.18632/aging.101700

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                TY  - JOUR
                AU  - Yang, Lin 
                AU  - Yang, Xingli 
                AU  - He, Wenzhuo 
                AU  - Liu, Shousheng 
                AU  - Jiang, Chang 
                AU  - Xie, Kunqian 
                AU  - Peng, Kunwei 
                AU  - You, Yafei 
                AU  - Zhang, Bei 
                AU  - Xia, Liangping 
                TI  - Comparisons of metastatic patterns of colorectal cancer among patients by age group: a population-based study
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101700
                DO  - 10.18632/aging.101700
                SP  - 4107
                EP  - 4119
                PY  - 
                AB  - Population-based evaluations of the incidence of metastatic colorectal cancer at diagnosis among different age groups are lacking. Therefore, we investigated the effects of age at diagnosis on metastatic colorectal cancer and patients’ prognoses. The Surveillance, Epidemiology, and End Results database was used to identify patients diagnosed with metastatic colorectal cancer. Multivariate Cox regression analyses were performed to identify factors associated with poor survival. The Kaplan–Meier analysis was used to estimate survival differences between the subgroups. We identified 30,333 adult patients diagnosed with metastatic colorectal cancer between 2010 and 2014. The younger and middle-aged groups had better survival than the older group when brain metastasis was not involved. The liver was the most common site of metastasis followed by the liver and lung combined. Age at diagnosis was an independent factor in patients’ survival. Survival differences between two and three-sites of metastases were found in the middle-aged and older groups but not in the younger group. No survival differences between three and four sites of metastases were found in any of the age groups. Therefore, the incidence and prognosis of metastatic sites for metastatic colorectal cancer varied by age group.
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Overexpression of FoxM1 predicts poor prognosis of intrahepatic cholangiocarcinoma

Lingyun Liu, Jian Wu, Yu Guo, Wenxuan Xie, Bin Chen, Yi Zhang, Shaoqiang Li, Yunpeng Hua, Baogang Peng, Shunli Shen,

https://doi.org/10.18632/aging.101706 pp 4120—4140

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Liu L, Wu J, Guo Y, Xie W, Chen B, Zhang Y, Li S, Hua Y, Peng B, Shen S, . Overexpression of FoxM1 predicts poor prognosis of intrahepatic cholangiocarcinoma. . 10:4120-4140. https://doi.org/10.18632/aging.101706

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                TY  - JOUR
                AU  - Liu, Lingyun 
                AU  - Wu, Jian 
                AU  - Guo, Yu 
                AU  - Xie, Wenxuan 
                AU  - Chen, Bin 
                AU  - Zhang, Yi 
                AU  - Li, Shaoqiang 
                AU  - Hua, Yunpeng 
                AU  - Peng, Baogang 
                AU  - Shen, Shunli 
                TI  - Overexpression of FoxM1 predicts poor prognosis of intrahepatic cholangiocarcinoma
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101706
                DO  - 10.18632/aging.101706
                SP  - 4120
                EP  - 4140
                PY  - 
                AB  - FoxM1 is an oncoprotein that is significantly overexpressed in many malignancies including hepatocellular carcinoma, but its role in intrahepatic cholangiocarcinoma (ICC) remains unclear. This study explores the expression of FoxM1 in human ICC, its relationships with clinical outcomes, and its role in the proliferation, migration, and invasion of ICC in vitro and in vivo. The results show that FoxM1 was markedly elevated in tumor tissues versus the paired peritumoral tissues. Overexpression of FoxM1 was correlated with multiple tumor nodules, tumor size &gt; 5 cm, positive lymph node metastasis and advanced TNM stage. Cox analysis revealed that overexpression of FoxM1 is an independent prognostic indicator for both the overall survival and disease-free survival of ICC patients after hepatectomy. Furthermore, up/downregulation of FoxM1 markedly promoted/inhibited ICC cell proliferation, migration, and invasion in vitro and in vivo. Bioinformatic analysis indicated that overexpression of FoxM1 resulted in the dysregulation of multiple signaling pathways in ICC, and selected components of some key signaling pathways such as c-Myc signaling were confirmed in vitro. In addition, overexpression of FoxM1 enhanced MMP-9 and MMP-2 protein expression in ICC cells. In conclusion, FoxM1 promotes ICC progression and is a reliable predictor of poor prognosis in ICC.
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Naringin targets Zeb1 to suppress osteosarcoma cell proliferation and metastasis

He Ming, Qiu Chuang, Wang Jiashi, Li Bin, Wang Guangbin, Ji Xianglu,

https://doi.org/10.18632/aging.101710 pp 4141—4151

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Ming H, Chuang Q, Jiashi W, Bin L, Guangbin W, Xianglu J, . Naringin targets Zeb1 to suppress osteosarcoma cell proliferation and metastasis. . 10:4141-4151. https://doi.org/10.18632/aging.101710

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                TY  - JOUR
                AU  - Ming, He 
                AU  - Chuang, Qiu 
                AU  - Jiashi, Wang 
                AU  - Bin, Li 
                AU  - Guangbin, Wang 
                AU  - Xianglu, Ji 
                TI  - Naringin targets Zeb1 to suppress osteosarcoma cell proliferation and metastasis
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101710
                DO  - 10.18632/aging.101710
                SP  - 4141
                EP  - 4151
                PY  - 
                AB  - Naringin, a citrus bioflavonoid, has anti-inflammatory actions and cardio- and neuroprotective effects. In addition, naringin exhibits multiple antitumor actions in several cancer types, including osteosarcoma, the most common type of bone cancer. Here, we show that naringin inhibits proliferation and invasion and induces apoptosis in human osteosarcoma cells by inhibiting zinc finger E-box binding homeobox 1 (Zeb1), a transcriptional repressor of epithelial differentiation involved in tumor metastasis. Our expression analyses confirm that Zeb1 is highly expressed in osteosarcoma specimens and cell lines. The effects of naringin, which included downregulation of Cyclin D1, MMP2, and bcl-2, where reproduced by siRNA-mediated Zeb1 silencing, whereas Zeb1 overexpression increased proliferation, migration, and Cyclin D1, MMP2, and bcl-2 levels. In addition, naringin administration reduced tumor nodule formation and attenuated the expression of the above proteins in the livers of mice injected with MG63 osteosarcoma cells. Our study provides preclinical evidence for the potential therapeutic application of naringin in the treatment of osteosarcoma.
                ER  -

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Mechanistic insight into hyaluronic acid and platelet-rich plasma-mediated anti-inflammatory and anti-apoptotic activities in osteoarthritic mice

Chi-Sheng Chiou, Chi-Ming Wu, Navneet Kumar Dubey, Wen-Cheng Lo, Feng-Chou Tsai, Tran Dang Xuan Tung, Wei-Ching Hung, Wei-Che Hsu, Wei-Hong Chen, Win-Ping Deng,

https://doi.org/10.18632/aging.101713 pp 4152—4165

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Chiou C, Wu C, Dubey NK, Lo W, Tsai F, Tung TDX, Hung W, Hsu W, Chen W, Deng W, . Mechanistic insight into hyaluronic acid and platelet-rich plasma-mediated anti-inflammatory and anti-apoptotic activities in osteoarthritic mice. . 10:4152-4165. https://doi.org/10.18632/aging.101713

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                TY  - JOUR
                AU  - Chiou, Chi-Sheng 
                AU  - Wu, Chi-Ming 
                AU  - Dubey, Navneet Kumar 
                AU  - Lo, Wen-Cheng 
                AU  - Tsai, Feng-Chou 
                AU  - Tung, Tran Dang Xuan 
                AU  - Hung, Wei-Ching 
                AU  - Hsu, Wei-Che 
                AU  - Chen, Wei-Hong 
                AU  - Deng, Win-Ping 
                TI  - Mechanistic insight into hyaluronic acid and platelet-rich plasma-mediated anti-inflammatory and anti-apoptotic activities in osteoarthritic mice
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101713
                DO  - 10.18632/aging.101713
                SP  - 4152
                EP  - 4165
                PY  - 
                AB  - Osteoarthritis (OA) poses a major clinical challenges owing to limited regenerative ability of diseased or traumatized chondrocytes in articular cartilage. Previous studies have determined the individual therapeutic efficacies of hyaluronic acid (HA) and platelet-rich plasma (PRP) on OA; however, the underlying mechanism is still lacking. Therefore, we investigated mechanistic approach of HA+PRP therapy on chondrocyte apoptosis in IL-1β+TNF-α (I+T) treated in vitro OA model, in addition to in vivo anterior cruciate ligament transection-OA mice model. MTT assay showed an enhanced chondrocyte proliferation and viability in HA+PRP-treated group, compared to I+T, I+T/HA, I+T/PRP, I+T/HA+PRP groups. Further, HA+PRP also significantly suppressed ROS, apoptotic cleaved caspase-3 and PARP, p53 and p21 and MMP-1; whereas, cell cycle modulatory proteins including p-ERK, cyclin B1, D1, and E2 were upregulated. The sub-G1 population and TUNEL assay confirmed the higher abundance of healthy chondrocytes in HA+PRP group. A significantly decreased ARS staining in HA+PRP group was also noted, indicating reduced cartilaginous matrix mineralization compared to other groups. Conclusively, compared to HA or PRP, the combined HA+PRP might be a promising therapy for articular cartilage regeneration in osteoarthritic pathology, possibly via augmented anti-inflammatory, anti-oxidative chondrocyte proliferation and inhibited MMP-1 activity and matrix calcification.
                ER  -

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Exercise training augments Sirt1-signaling and attenuates cardiac inflammation in D-galactose induced-aging rats

Wei-Kung Chen, Ying-Lan Tsai, Marthandam Asokan Shibu, Chia-Yao Shen, Shu Nu Chang-Lee, Ray-Jade Chen, Chun-Hsu Yao, Bo Ban, Wei-Wen Kuo, Chih-Yang Huang,

https://doi.org/10.18632/aging.101714 pp 4166—4174

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Chen W, Tsai Y, Shibu MA, Shen C, Chang-Lee SN, Chen R, Yao C, Ban B, Kuo W, Huang C, . Exercise training augments Sirt1-signaling and attenuates cardiac inflammation in D-galactose induced-aging rats. . 10:4166-4174. https://doi.org/10.18632/aging.101714

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                TY  - JOUR
                AU  - Chen, Wei-Kung 
                AU  - Tsai, Ying-Lan 
                AU  - Shibu, Marthandam Asokan 
                AU  - Shen, Chia-Yao 
                AU  - Chang-Lee, Shu Nu 
                AU  - Chen, Ray-Jade 
                AU  - Yao, Chun-Hsu 
                AU  - Ban, Bo 
                AU  - Kuo, Wei-Wen 
                AU  - Huang, Chih-Yang 
                TI  - Exercise training augments Sirt1-signaling and attenuates cardiac inflammation in D-galactose induced-aging rats
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101714
                DO  - 10.18632/aging.101714
                SP  - 4166
                EP  - 4174
                PY  - 
                AB  - Exercise is known to be beneficial in controlling aging associated disorders however, the consequence of long-term exercise on cardiac health among aging population is not much clear. In this study the protective effect of exercise on aging associated cardiac disorders was determined using a D-galactose-induced aging model. Eight weeks old Sprague Dawley rats were given intraperitoneal injection of 150 mL/kg D-galactose. Swimming exercise was provided in warm water for 60 min/day for five days per week. Hematoxylin and eosin staining of cardiac tissue sections revealed cardiomyocyte disarrangements in the aging rat hearts but long-term exercise training showed improvements in the cardiac histology. Exercise training also enhanced the expression levels of proteins such as SIRT1, PGC-1α and AMPKα1 that are associated with energy homeostasis and further suppressed aging associated inflammatory cytokines. Our results show that long-term exercise training potentially enhances SIRT1 associated anti-aging signaling and provide cardio-protection against aging.
                ER  -

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Melatonin alleviates meiotic defects in fetal mouse oocytes induced by Di (2-ethylhexyl) phthalate in vitro

Zhong-Yi Sun, Pan Zhang, Jun-Jie Wang, Jing-Cai Liu, Lan Li, Wei Shen, Qiu-Yue Zhai,

https://doi.org/10.18632/aging.101715 pp 4175—4187

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Sun Z, Zhang P, Wang J, Liu J, Li L, Shen W, Zhai Q, . Melatonin alleviates meiotic defects in fetal mouse oocytes induced by Di (2-ethylhexyl) phthalate in vitro. . 10:4175-4187. https://doi.org/10.18632/aging.101715

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Provider: 
 TY - JOUR
 AU - Sun, Zhong-Yi 
 AU - Zhang, Pan 
 AU - Wang, Jun-Jie 
 AU - Liu, Jing-Cai 
 AU - Li, Lan 
 AU - Shen, Wei 
 AU - Zhai, Qiu-Yue 
 TI - Melatonin alleviates meiotic defects in fetal mouse oocytes induced by Di (2-ethylhexyl) phthalate in vitro
 JO - 
 JA - 
 VL - 10
 IS - 12
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101715
 DO - 10.18632/aging.101715
 SP - 4175
 EP - 4187
 PY - 
 AB - Di (2-ethylhexyl) phthalate (DEHP), an estrogen-like compound that is a ubiquitous environmental contaminant, has been reported to adversely affect human and mammalian reproduction. Many studies have found that exposure to DEHP during pregnancy perturbs female germ cell meiosis and is detrimental to oogenesis. Previous studies have demonstrated that melatonin (MLT) is beneficial to reproductive endocrinology, oogenesis, and embryonic development as the ability to antioxidative and antiapoptotic. However, whether the meiotic defect of germ cells exposed to DEHP could be rescued by MLT is not clear. Here, we cultured 12.5 days post coitum (dpc) fetal mouse ovaries for 6 days, exposed them to 100 μM DEHP with or without 1 μM MLT in vitro.. The results showed that DEHP exposure induced the abnormal formation of DNA double-strand breaks (DSBs), and inhibited the repair of DSBs during meiotic recombination. In addition, we found defective oocytes were prone to undergo apoptosis. Notably, this defect could be remarkably ameliorated by the addition of MLT via a reduction of the levels of reactive oxygen species and an inhibition of apoptosis. In conclusion, our data revealed that MLT had a protective action against the meiotic deterioration of fetal oocytes induced by DEHP in the mouse in vitro.
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Fluoxetine-mediated inhibition of endoplasmic reticulum stress is involved in the neuroprotective effects of Parkinson’s disease

Tao Peng, Xiaoyan Liu, Jingtao Wang, Yu Liu, Zhenqiang FU, Xingrong Ma, Junmin Li, Guifang Sun, Yangfei Ji, Jingjing Lu, Wencui Wan, Hong Lu,

https://doi.org/10.18632/aging.101716 pp 4188—4196

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Peng T, Liu X, Wang J, Liu Y, FU Z, Ma X, Li J, Sun G, Ji Y, Lu J, Wan W, Lu H, . Fluoxetine-mediated inhibition of endoplasmic reticulum stress is involved in the neuroprotective effects of Parkinson’s disease. . 10:4188-4196. https://doi.org/10.18632/aging.101716

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                TY  - JOUR
                AU  - Peng, Tao 
                AU  - Liu, Xiaoyan 
                AU  - Wang, Jingtao 
                AU  - Liu, Yu 
                AU  - FU, Zhenqiang 
                AU  - Ma, Xingrong 
                AU  - Li, Junmin 
                AU  - Sun, Guifang 
                AU  - Ji, Yangfei 
                AU  - Lu, Jingjing 
                AU  - Wan, Wencui 
                AU  - Lu, Hong 
                TI  - Fluoxetine-mediated inhibition of endoplasmic reticulum stress is involved in the neuroprotective effects of Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101716
                DO  - 10.18632/aging.101716
                SP  - 4188
                EP  - 4196
                PY  - 
                AB  - Background: Accumulating evidence suggests that Fluoxetine (FLX), an anti-depressant drug, has broad neurobiological functions and neuroprotective effects in central nervous system injury, but its roles in Parkinson's disease (PD) remain unclear. In this study, we aimed to evaluate whether fluoxetine attenuates rotenone-induced neurodegeneration in PD.Methods: Male Sprague-Dawley rats were randomly allocated to control, rotenone-treated, rotenone + FLX-treated and FLX-treated groups. Behavioral tests including open field behavioral test and catalepsy measurement were taken to evaluate neurological behavioral measurements. Apoptosis was detected by TUNEL assay. Endoplasmic reticulum (ER)-related gene expressions were detected by qRT-PCR and western blot. Immunohistochemistry was performed to assess dopaminergic neuronal degeneration.Results: We demonstrated that pretreatment with FLX (10.0 mg/kg, i.p.) significantly ameliorated the catalepsy symptom and increased locomotor activity. In addition, FLX markedly reversed the loss of dopaminergic neurons and suppressed the X‑box‑binding protein 1 (XBP1)/caspase-3-activated ER stress. Furthermore, FLX inhibited rotenone-mediated neurodegeneration through caspase-3-mediated neuronal apoptosis.Conclusion: Taken together, our findings indicate that FLX has beneficial neuroprotective effects in PD and FLX might be a potential therapeutic agent for the treatment of PD. In light of its favorable properties, FLX should be evaluated in the treatment of PD as well as related neurologic disorders.
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Hyperoside attenuates renal aging and injury induced by D-galactose via inhibiting AMPK-ULK1 signaling-mediated autophagy

Buhui Liu, Yue Tu, Weiming He, Yinglu Liu, Wei Wu, Qijun Fang, Haitao Tang, Renmao Tang, Ziyue Wan, Wei Sun, Yigang Wan,

https://doi.org/10.18632/aging.101723 pp 4197—4212

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Liu B, Tu Y, He W, Liu Y, Wu W, Fang Q, Tang H, Tang R, Wan Z, Sun W, Wan Y, . Hyperoside attenuates renal aging and injury induced by D-galactose via inhibiting AMPK-ULK1 signaling-mediated autophagy. . 10:4197-4212. https://doi.org/10.18632/aging.101723

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                TY  - JOUR
                AU  - Liu, Buhui 
                AU  - Tu, Yue 
                AU  - He, Weiming 
                AU  - Liu, Yinglu 
                AU  - Wu, Wei 
                AU  - Fang, Qijun 
                AU  - Tang, Haitao 
                AU  - Tang, Renmao 
                AU  - Wan, Ziyue 
                AU  - Sun, Wei 
                AU  - Wan, Yigang 
                TI  - Hyperoside attenuates renal aging and injury induced by D-galactose via inhibiting AMPK-ULK1 signaling-mediated autophagy
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101723
                DO  - 10.18632/aging.101723
                SP  - 4197
                EP  - 4212
                PY  - 
                AB  - The kidney is a typical organ undergoing age and injury. Hyperoside is reported to be useful for preventing aging induced by D-galactose (D-gal). However, therapeutic mechanisms remain unclear. We thereby aimed to verify whether hyperoside, compared to vitamin E (VE), could alleviate renal aging and injury by regulating autophagic activity and its related signaling pathways. In vivo, rats were administered with either hyperoside or VE after renal aging modeling induced by D-gal. Changes in renal aging and injury markers, autophagic activity and AMPK-ULK1 signaling pathway in the kidneys were analysed. In vitro, the NRK-52E cells exposed to D-gal were used to investigate regulative actions of hyperoside and VE on cell viability, renal tubular cellular aging markers, autophagic activity and its related signaling pathways by histomorphometry, immunohistochemistry, immunofluorescence, lentiviral transfection and Western blot. Aging and injury in the kidneys and renal tubular cells induced by D-gal were ameliorated by hyperoside and VE. Hyperoside and VE inhibited autophagic activity through mTOR-independent and AMPK-ULK1 signaling pathways. Hyperoside, as a component of phytomedicine similar to VE, attenuated renal aging and injury induced by D-gal via inhibiting AMPK-ULK1-mediated autophagy. This study provides the first evidence that hyperoside contributes to the prevention of age-associated renal injury.
                ER  -

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Caloric restriction is associated with preservation of muscle strength in experimental cancer cachexia

Stef Levolger, Sandra van den Engel, Gisela Ambagtsheer, Jan N.M. IJzermans, Ron W.F. de Bruin,

https://doi.org/10.18632/aging.101724 pp 4213—4223

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Levolger S, van den Engel S, Ambagtsheer G, IJzermans JN, de Bruin RW, . Caloric restriction is associated with preservation of muscle strength in experimental cancer cachexia. . 10:4213-4223. https://doi.org/10.18632/aging.101724

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                TY  - JOUR
                AU  - Levolger, Stef 
                AU  - van den Engel, Sandra 
                AU  - Ambagtsheer, Gisela 
                AU  - IJzermans, Jan N.M. 
                AU  - de Bruin, Ron W.F. 
                TI  - Caloric restriction is associated with preservation of muscle strength in experimental cancer cachexia
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101724
                DO  - 10.18632/aging.101724
                SP  - 4213
                EP  - 4223
                PY  - 
                AB  - Caloric restriction increases lifespan and healthspan, and limits age-associated muscle wasting. In this study, we investigate the impact of 30% caloric restriction (CR) in a murine cancer cachexia model. Forty CD2F1 mice were allocated as C26 tumor-bearing (TB) + ad libitum food intake (dietary reference intake [DRI]), TB CR, non-TB (NTB) CR, or NTB matched intake (MI). TB groups were inoculated subcutaneously with 0.5x106 C26 cells 14 days after initiating CR. Bodyweight, food intake, and grip-strength were recorded periodically. Gastrocnemius (GCM) and tibialis anterior (TA) muscles were resected and weighed 3 weeks after tumor inoculation. mRNA expression of MuRF1, Atrogin-1, myogenin, and MyoD was determined. At tumor inoculation, the mean body weight of TB CR was 88.6% of initial body weight and remained stable until sacrifice. TB DRI showed wasting before sacrifice. TB groups experienced muscle wasting compared with NTB MI. Grip-strength change was less severe in TB CR. Expression of MuRF1, Atrogin-1, and MyoD was similar between TB DRI and both CR groups. Expression of myogenin was increased in CR groups. In conclusion, caloric restriction limits loss of muscle strength but has no impact on muscle mass despite significant loss of body weight in an experimental cancer-associated cachexia model.
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ΔNp63 promotes IGF1 signalling through IRS1 in squamous cell carcinoma

Valentina Frezza, Claudia Fierro, Elena Gatti, Angelo Peschiaroli, Anna Maria Lena, Margherita Annicchiarico Petruzzelli, Eleonora Candi, Lucia Anemona, Alessandro Mauriello, Pier Giuseppe Pelicci, Gerry Melino, Francesca Bernassola,

https://doi.org/10.18632/aging.101725 pp 4224—4240

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Frezza V, Fierro C, Gatti E, Peschiaroli A, Lena AM, Petruzzelli MA, Candi E, Anemona L, Mauriello A, Pelicci PG, Melino G, Bernassola F, . ΔNp63 promotes IGF1 signalling through IRS1 in squamous cell carcinoma. . 10:4224-4240. https://doi.org/10.18632/aging.101725

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                TY  - JOUR
                AU  - Frezza, Valentina 
                AU  - Fierro, Claudia 
                AU  - Gatti, Elena 
                AU  - Peschiaroli, Angelo 
                AU  - Lena, Anna Maria 
                AU  - Petruzzelli, Margherita Annicchiarico 
                AU  - Candi, Eleonora 
                AU  - Anemona, Lucia 
                AU  - Mauriello, Alessandro 
                AU  - Pelicci, Pier Giuseppe 
                AU  - Melino, Gerry 
                AU  - Bernassola, Francesca 
                TI  - ΔNp63 promotes IGF1 signalling through IRS1 in squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101725
                DO  - 10.18632/aging.101725
                SP  - 4224
                EP  - 4240
                PY  - 
                AB  - Accumulating evidence has proved that deregulation of ΔNp63 expression plays an oncogenic role in head and neck squamous cell carcinomas (HNSCCs). Besides p63, the type 1-insulin-like growth factor (IGF) signalling pathway has been implicated in HNSCC development and progression. Most insulin/IGF1 signalling converges intracellularly onto the protein adaptor insulin receptor substrate-1 (IRS-1) that transmits signals from the receptor to downstream effectors, including the PI3K/AKT and the MAPK kinase pathways, which, ultimately, promote proliferation, invasion, and cell survival. Here we report that p63 directly controls IRS1 transcription and cellular abundance and fosters the PI3K/AKT and MAPK downstream signalling pathways. Inactivation of ΔNp63 expression indeed reduces tumour cell responsiveness to IGF1 stimulation, and inhibits the growth potential of HNSCC cells. In addition, a positive correlation was observed between p63 and IRS1 expression in human HNSCC tissue arrays and in publicly available gene expression data. Our findings indicate that aberrant expression of ΔNp63 in HNSSC may act as an oncogenic stimulus by altering the IGF signalling pathway.
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Circulating insulin-like growth factor-1: a new clue in the pathogenesis of age-related macular degeneration

Niccolò Castellino, Antonio Longo, Teresio Avitabile, Andrea Russo, Matteo Fallico, Vincenza Bonfiglio, Mario Damiano Toro, Robert Rejdak, Katarzyna Nowomiejska, Paolo Murabito, Claudio Furino, Michele Reibaldi,

https://doi.org/10.18632/aging.101727 pp 4241—4247

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Castellino N, Longo A, Avitabile T, Russo A, Fallico M, Bonfiglio V, Toro MD, Rejdak R, Nowomiejska K, Murabito P, Furino C, Reibaldi M, . Circulating insulin-like growth factor-1: a new clue in the pathogenesis of age-related macular degeneration. . 10:4241-4247. https://doi.org/10.18632/aging.101727

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                TY  - JOUR
                AU  - Castellino, Niccolò 
                AU  - Longo, Antonio 
                AU  - Avitabile, Teresio 
                AU  - Russo, Andrea 
                AU  - Fallico, Matteo 
                AU  - Bonfiglio, Vincenza 
                AU  - Toro, Mario Damiano 
                AU  - Rejdak, Robert 
                AU  - Nowomiejska, Katarzyna 
                AU  - Murabito, Paolo 
                AU  - Furino, Claudio 
                AU  - Reibaldi, Michele 
                TI  - Circulating insulin-like growth factor-1: a new clue in the pathogenesis of age-related macular degeneration
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101727
                DO  - 10.18632/aging.101727
                SP  - 4241
                EP  - 4247
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Castellino, Niccolò 
                AU  - Longo, Antonio 
                AU  - Avitabile, Teresio 
                AU  - Russo, Andrea 
                AU  - Fallico, Matteo 
                AU  - Bonfiglio, Vincenza 
                AU  - Toro, Mario Damiano 
                AU  - Rejdak, Robert 
                AU  - Nowomiejska, Katarzyna 
                AU  - Murabito, Paolo 
                AU  - Furino, Claudio 
                AU  - Reibaldi, Michele 
                TI  - Circulating insulin-like growth factor-1: a new clue in the pathogenesis of age-related macular degeneration
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101727
                DO  - 10.18632/aging.101727
                SP  - 4241
                EP  - 4247
                PY  - 
                AB  - In order to investigate Insulin-like growth factor-1 (IGF-1) blood levels in male and female age-matched patients affected by early, intermediate, neovascular age related macular degeneration (AMD) and healthy subjects (no AMD) were enrolled in a prospective, observational study. All patients enrolled were classified according to 4 stages classification of AMD from Age-related eye disease study (AREDS). Each subject underwent a complete ophthalmic examination including best corrected visual acuity (BCVA), applanation tonometry, slit-lamp biomicroscopic examination, color fundus photography, optical coherence tomography (OCT) and, if needed, fluorescein angiography. Overall, 224 anti-VEGF naïve subjects including 56 patients in early AMD group, 56 patients in intermediate AMD group, 56 patients in neovascular AMD group and 56 patients in no AMD group were recruited. For each group 28 male patients and 28 female patients were enrolled. IGF-1 hematic levels were significantly higher (p&lt;0.005) in the neovascular AMD group and in the intermediate AMD group in comparison to no AMD group; no significant difference between early AMD group and no AMD group was found. Our analysis has shown an increment of IGF-1 levels in both neovascular and intermediate stage of AMD supporting the hypothesis that IGF-1 may play a role in the pathogenesis of AMD.
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How I treat elderly patients with plasma cell dyscrasias

Maria Gavriatopoulou, Despoina Fotiou, Ioannis Ntanasis-Stathopoulos, Efstathios Kastritis, Evangelos Terpos, Meletios Athanasios Dimopoulos,

https://doi.org/10.18632/aging.101707 pp 4248—4268

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Gavriatopoulou M, Fotiou D, Ntanasis-Stathopoulos I, Kastritis E, Terpos E, Dimopoulos MA, . How I treat elderly patients with plasma cell dyscrasias. . 10:4248-4268. https://doi.org/10.18632/aging.101707

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                TY  - JOUR
                AU  - Gavriatopoulou, Maria 
                AU  - Fotiou, Despoina 
                AU  - Ntanasis-Stathopoulos, Ioannis 
                AU  - Kastritis, Efstathios 
                AU  - Terpos, Evangelos 
                AU  - Dimopoulos, Meletios Athanasios 
                TI  - How I treat elderly patients with plasma cell dyscrasias
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101707
                DO  - 10.18632/aging.101707
                SP  - 4248
                EP  - 4268
                PY  - 
                AB  - Plasma cell dyscrasias are a rare heterogeneous group of hematological disorders which are more prevalent in the older part of the population. The introduction of novel agents, improved understanding of disease biology and better supportive management have improved outcomes considerably and in the era of the aging population the question of how to best manage older patients with plasma cell dyscrasias has never been more relevant. Data on how to treat these patients comes mostly from subgroup analysis as they are underrepresented in clinical trials. This review will cover issues, available evidence and recommendations relevant to diagnosis and management of the older patients with Multiple Myeloma (MM), Waldenstrom Macroglobulinemia (WM) and systemic AL Amyloidosis. What will become increasingly evident is the need to develop and establish the use of disease-specific geriatric assessment (GA) tools. Frailty status assessment using GA tools and moving away from making decisions based merely on chronological age will allow setting clear treatment goals and consequently achieving an optimum balance between effectiveness and toxicity for this complex and heterogeneous group of patients.
                ER  -

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Protein synthesis and quality control in aging

Aleksandra S. Anisimova, Alexander I. Alexandrov, Nadezhda E. Makarova, Vadim N. Gladyshev, Sergey E. Dmitriev,

https://doi.org/10.18632/aging.101721 pp 4269—4288

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Anisimova AS, Alexandrov AI, Makarova NE, Gladyshev VN, Dmitriev SE, . Protein synthesis and quality control in aging. . 10:4269-4288. https://doi.org/10.18632/aging.101721

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                TY  - JOUR
                AU  - Anisimova, Aleksandra S. 
                AU  - Alexandrov, Alexander I. 
                AU  - Makarova, Nadezhda E. 
                AU  - Gladyshev, Vadim N. 
                AU  - Dmitriev, Sergey E. 
                TI  - Protein synthesis and quality control in aging
                JO  - 
                JA  - 
                VL  - 10
                IS  - 12
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101721
                DO  - 10.18632/aging.101721
                SP  - 4269
                EP  - 4288
                PY  - 
                AB  - Aging is characterized by the accumulation of damage and other deleterious changes, leading to the loss of functionality and fitness. Age-related changes occur at most levels of organization of a living organism (molecular, organellar, cellular, tissue and organ). However, protein synthesis is a major biological process, and thus understanding how it changes with age is of paramount importance. Here, we discuss the relationships between lifespan, aging, protein synthesis and translational control, and expand this analysis to the various aspects of proteome behavior in organisms with age. Characterizing the consequences of changes in protein synthesis and translation fidelity, and determining whether altered translation is pathological or adaptive is necessary for understanding the aging process, as well as for developing approaches to target dysfunction in translation as a strategy for extending lifespan.
                ER  -

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Paradoxes of senolytics

Mikhail V. Blagosklonny,

https://doi.org/10.18632/aging.101750 pp 4289—4293

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Correction: The fasting blood glucose and long non-coding RNA SNHG8 predict poor prognosis in patients with gastric carcinoma after radical gastrectomy

Yunchai Lin, Dan Hu, Qiang Zhou, Xiandong Lin, Jinxiu Lin, Feng Peng,

https://doi.org/10.18632/aging.101755 pp 4294

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Lin Y, Hu D, Zhou Q, Lin X, Lin J, Peng F, . Correction: The fasting blood glucose and long non-coding RNA SNHG8 predict poor prognosis in patients with gastric carcinoma after radical gastrectomy. . 10:4294-4294. https://doi.org/10.18632/aging.101755

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Volume 10, Issue 12

About the Cover

Editorials

Yosef Sarne,

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Itamar Lerner, Ravi Sojitra, Mark Gluck,

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