Volume 10, Issue 7

Anderson E, Cochrane A, Golding J, Nowicki S, . Locus of control as a modifiable risk factor for cognitive function in midlife. . 10:1542-1555. https://doi.org/10.18632/aging.101490

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                TY  - JOUR
                AU  - Anderson, Emma 
                AU  - Cochrane, Alice 
                AU  - Golding, Jean 
                AU  - Nowicki, Stephen 
                TI  - Locus of control as a modifiable risk factor for cognitive function in midlife
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101490
                DO  - 10.18632/aging.101490
                SP  - 1542
                EP  - 1555
                PY  - 
                AB  - Few modifiable risk factors for cognitive decline have been identified. Despite an external locus of control (LoC) being adversely associated with many psychological and physical health outcomes, few studies have examined whether it is related to cognitive function in adulthood. In 1178 women from the Avon Longitudinal Study of Parents and Children, we examined whether LoC, and change in LoC over time, is associated with cognitive function in midlife. LoC was prospectively measured at mean ages 30 and 48 years using the validated Nowicki-Strickland scale. Cognitive function was examined at mean age 51 years. At both time points, greater externality was associated with lower cognitive function. For example, the group of women classified as being external at mean age 48 years had, on average, a 0.18 lower cognitive function score (95% CI: (0.11 to 0.25) than the group classified as being internal (p&lt;0.001). Participants who changed from external to internal over time, on average, had better cognitive function than those who remained external or changed to become external. In summary, an external LoC may be detrimental to cognitive function. Thus, interventions to increase internality may help to minimise the adverse consequences on cognitive health later in life.
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Nicotine exposure impairs germ cell development in human fetal ovaries cultured in vitro

Shun-Feng Cheng, Xun-Si Qin, Ze-Li Han, Xiao-Feng Sun, Yan-Ni Feng, Fan Yang, Wei Ge, Lan Li, Yong Zhao, Massimo De Felici, Shu-Hua Zou, Yi Zhou, Wei Shen,

https://doi.org/10.18632/aging.101492 pp 1556—1574

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Cheng S, Qin X, Han Z, Sun X, Feng Y, Yang F, Ge W, Li L, Zhao Y, De Felici M, Zou S, Zhou Y, Shen W, . Nicotine exposure impairs germ cell development in human fetal ovaries cultured in vitro. . 10:1556-1574. https://doi.org/10.18632/aging.101492

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 TY - JOUR
 AU - Cheng, Shun-Feng 
 AU - Qin, Xun-Si 
 AU - Han, Ze-Li 
 AU - Sun, Xiao-Feng 
 AU - Feng, Yan-Ni 
 AU - Yang, Fan 
 AU - Ge, Wei 
 AU - Li, Lan 
 AU - Zhao, Yong 
 AU - De Felici, Massimo 
 AU - Zou, Shu-Hua 
 AU - Zhou, Yi 
 AU - Shen, Wei 
 TI - Nicotine exposure impairs germ cell development in human fetal ovaries cultured in vitro
 JO - 
 JA - 
 VL - 10
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101492
 DO - 10.18632/aging.101492
 SP - 1556
 EP - 1574
 PY - 
 AB - In the present paper, we found that human fetal ovaries (at ~16 weeks) express the transcripts for several subunits of the nicotinic acetylcholine receptor (nAChR). Exposure to the drug in vitro resulted in the marked increase of apoptosis in the ovaries in a time and dose-dependent manner. Evidence that adverse nicotine effects are potentially due to an increased level of reactive oxygen species (ROS) and consequent DNA damage, both in the ovarian somatic cells and germ cells, are reported. After 4 days of culture, exposure to 1 mM and 10 mM nicotine caused a 50% and 75% decrease, respectively, in the number of oogonia/oocytes present in the fetal ovaries. These results represent the first indication that nicotine may directly cause apoptosis in cells of the fetal human ovary and may lead to a reduction of the ovarian reserve oocytes and consequent precocious menopause in mothers smoking during pregnancy.
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Hybrid complexes of high and low molecular weight hyaluronan delay in vitro replicative senescence of mesenchymal stromal cells: a pilot study for future therapeutic application

Nicola Alessio, Antonietta Stellavato, Tiziana Squillaro, Stefania Del Gaudio, Giovanni Di Bernardo, Gianfranco Peluso, Mario De Rosa, Chiara Schiraldi, Umberto Galderisi,

https://doi.org/10.18632/aging.101493 pp 1575—1585

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Alessio N, Stellavato A, Squillaro T, Del Gaudio S, Di Bernardo G, Peluso G, De Rosa M, Schiraldi C, Galderisi U, . Hybrid complexes of high and low molecular weight hyaluronan delay in vitro replicative senescence of mesenchymal stromal cells: a pilot study for future therapeutic application. . 10:1575-1585. https://doi.org/10.18632/aging.101493

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                TY  - JOUR
                AU  - Alessio, Nicola 
                AU  - Stellavato, Antonietta 
                AU  - Squillaro, Tiziana 
                AU  - Del Gaudio, Stefania 
                AU  - Di Bernardo, Giovanni 
                AU  - Peluso, Gianfranco 
                AU  - De Rosa, Mario 
                AU  - Schiraldi, Chiara 
                AU  - Galderisi, Umberto 
                TI  - Hybrid complexes of high and low molecular weight hyaluronan delay in vitro replicative senescence of mesenchymal stromal cells: a pilot study for future therapeutic application
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101493
                DO  - 10.18632/aging.101493
                SP  - 1575
                EP  - 1585
                PY  - 
                AB  - Mesenchymal stem cells, a subpopulation of mesenchymal stromal cells (MSCs), are present in the stroma of several tissues. MSC in vitro cultivation for clinical treatments may greatly affect MSC properties. A primary handicap is replicative senescence that impairs MSC functions. Hyaluronan (HA) is present in the extracellular matrix that composes the stem cell niche environment and is under investigation as a key factor for in vitro stem cell growth. We evaluated the effect on MSC cultivation of HA hybrid cooperative complexes (HCC) that are obtained from high (H) and low (L) weight molecules (NAHYCO™). We compared this HCC with H-HA and L-HA. We investigated the effects of these HAs on proliferation, cell cycle, apoptosis, senescence, and differentiation following the addition of the polymer solutions in the culture media at concentrations that did not drastically modify the medium viscosity. Interestingly, 0,16% HCC significantly delayed the senescence compared with the controls. This occurred without alteration of the cell cycle, cytotoxicity, or apoptosis. HCCs also promoted adipogenic and chondrogenic differentiation. Our finding could suggest a potential functional role of HCC above the updated scientific reports of its effects and pave the way to optimization of MSC cultivation for therapeutic application.
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Resveratrol increases resistance of mouse oocytes to postovulatory aging in vivo

Qiu-Xia Liang, Yi-Hua Lin, Chun-Hui Zhang, Hong-Mei Sun, Liang Zhou, Heide Schatten, Qing-Yuan Sun, Wei-Ping Qian,

https://doi.org/10.18632/aging.101494 pp 1586—1596

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Liang Q, Lin Y, Zhang C, Sun H, Zhou L, Schatten H, Sun Q, Qian W, . Resveratrol increases resistance of mouse oocytes to postovulatory aging in vivo. . 10:1586-1596. https://doi.org/10.18632/aging.101494

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 TY - JOUR
 AU - Liang, Qiu-Xia 
 AU - Lin, Yi-Hua 
 AU - Zhang, Chun-Hui 
 AU - Sun, Hong-Mei 
 AU - Zhou, Liang 
 AU - Schatten, Heide 
 AU - Sun, Qing-Yuan 
 AU - Qian, Wei-Ping 
 TI - Resveratrol increases resistance of mouse oocytes to postovulatory aging in vivo
 JO - 
 JA - 
 VL - 10
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101494
 DO - 10.18632/aging.101494
 SP - 1586
 EP - 1596
 PY - 
 AB - After ovulation, metaphase II oocytes undergo a time-dependent deterioration in vivo or in vitro, which is referred to as postovulatory oocyte aging, a process during which a series of deleterious molecular and cellular changes occur. In this study, we found that short-term injection of resveratrol (3,5,4'-trihydroxystilbene) effectively ameliorated oxidative stress-induced damage in postovulatory oocyte aging of middle-aged mice in vivo. Resveratrol induced changes that delayed the aging-induced oocyte deterioration including the elevated expression of the anti-aging molecule Sirtuin 1 (SIRT1); it reduced intracellular reactive oxygen species (ROS) level, and improved mitochondria function. In addition, these beneficial changes may also help to prevent apoptosis. Taken together, our data suggest that resveratrol can effectively protect against postovulatory oocyte aging in vivo primarily by preventing ROS production.
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Aging exacerbates mortality of Acinetobacter baumannii pneumonia and reduces the efficacies of antibiotics and vaccine

Hao Gu, Dong Liu, Xi Zeng, Liu-Sheng Peng, Yue Yuan, Zhi-Fu Chen, Quan-Ming Zou, Yun Shi,

https://doi.org/10.18632/aging.101495 pp 1597—1608

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Gu H, Liu D, Zeng X, Peng L, Yuan Y, Chen Z, Zou Q, Shi Y, . Aging exacerbates mortality of Acinetobacter baumannii pneumonia and reduces the efficacies of antibiotics and vaccine. . 10:1597-1608. https://doi.org/10.18632/aging.101495

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 TY - JOUR
 AU - Gu, Hao 
 AU - Liu, Dong 
 AU - Zeng, Xi 
 AU - Peng, Liu-Sheng 
 AU - Yuan, Yue 
 AU - Chen, Zhi-Fu 
 AU - Zou, Quan-Ming 
 AU - Shi, Yun 
 TI - Aging exacerbates mortality of Acinetobacter baumannii pneumonia and reduces the efficacies of antibiotics and vaccine
 JO - 
 JA - 
 VL - 10
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101495
 DO - 10.18632/aging.101495
 SP - 1597
 EP - 1608
 PY - 
 AB - Pneumonia caused by Acinetobacter baumannii has become a serious threat to the elderly. However, there are no experimental studies on the relevance between aging and A. baumannii infections. Here, we established an aged pneumonia mouse model by non-invasive intratracheal inoculation with A. baumannii. Higher mortality was observed in aged mice along with increased bacterial burdens and more severe lung injury. Increased inflammatory cell infiltration and enhanced pro-inflammatory cytokines at 24 hours post infection were detected in aged mice than those in young mice. Moreover, infected aged mice had lower myeloperoxidase levels in lungs and less reactive oxygen species-positive neutrophils in bronchoalveolar lavage fluid compared with infected young mice. Reduced efficacy of imipenem/cilastatin against A. baumannii was detected in aged mice. Vaccination of formalin-fixed A. baumannii provided 100% protection in young mice, whereas the efficacy of vaccine was completely diminished in aged mice. In conclusion, aging increased susceptibility to A. baumannii infection and impaired efficacies of antibiotics and vaccine. The aged mice model of A. baumannii pneumonia is a suitable model to study the effects of aging on A. baumannii infection and assess the efficacies of antibiotics and vaccines against A. baumannii for the elderly.
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Signatures of photo-aging and intrinsic aging in skin were revealed by transcriptome network analysis

Byuri Angela Cho, Seong-Keun Yoo, Jeong-Sun Seo,

https://doi.org/10.18632/aging.101496 pp 1609—1626

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Cho BA, Yoo S, Seo J, . Signatures of photo-aging and intrinsic aging in skin were revealed by transcriptome network analysis. . 10:1609-1626. https://doi.org/10.18632/aging.101496

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                TY  - JOUR
                AU  - Cho, Byuri Angela 
                AU  - Yoo, Seong-Keun 
                AU  - Seo, Jeong-Sun 
                TI  - Signatures of photo-aging and intrinsic aging in skin were revealed by transcriptome network analysis
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101496
                DO  - 10.18632/aging.101496
                SP  - 1609
                EP  - 1626
                PY  - 
                AB  - There are various factors that alter physiological characteristics in skin. Elucidating the underlying mechanism of transcriptional alterations by intrinsic and extrinsic factors may lead us to understand the aging process of skin. To identify the transcriptomic changes of the aging skin, we analyzed publicly available RNA sequencing data from Genotype-Tissue Expression (GTEx) project. GTEx provided RNA sequencing data of suprapubic (n=228) and lower leg (n=349) skins, which are photo-protected and photo–damaged. Using differentially expressed gene analysis and weighted gene co-expression network analysis, we characterized transcriptomic changes due to UV exposure and aging. Genes involved in skin development such as epidermal differentiation complex component (SPRR and LCE families), vasculature development (TGFBR1, TGFBR2, TGFBR3, KDR, FGF2, and VEGFC), and matrix metalloproteinase (MMP2, MMP3, MMP8, MMP10, and MMP13) were up-regulated by UV exposure. Also, down-regulated lipid metabolism and mitochondrial biogenesis were observed in photo-damaged skin. Moreover, wound healing process was universally down-regulated in suprapubic and lower leg with aging and further down-regulation of lipid metabolism and up-regulation of vasculature development were found as photo-aging signatures. In this study, dynamic transcriptomic alterations were observed in aged skin. Hence, our findings may help to discover a potential therapeutic target for skin rejuvenation.
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A three-long non-coding RNA-expression-based risk score system can better predict both overall and recurrence-free survival in patients with small hepatocellular carcinoma

Jingxian Gu, Xing Zhang, Runchen Miao, Xiaohua Ma, Xiaohong Xiang, Yunong Fu, Chang Liu, Wenquan Niu, Kai Qu,

https://doi.org/10.18632/aging.101497 pp 1627—1639

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Gu J, Zhang X, Miao R, Ma X, Xiang X, Fu Y, Liu C, Niu W, Qu K, . A three-long non-coding RNA-expression-based risk score system can better predict both overall and recurrence-free survival in patients with small hepatocellular carcinoma. . 10:1627-1639. https://doi.org/10.18632/aging.101497

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                TY  - JOUR
                AU  - Gu, Jingxian 
                AU  - Zhang, Xing 
                AU  - Miao, Runchen 
                AU  - Ma, Xiaohua 
                AU  - Xiang, Xiaohong 
                AU  - Fu, Yunong 
                AU  - Liu, Chang 
                AU  - Niu, Wenquan 
                AU  - Qu, Kai 
                TI  - A three-long non-coding RNA-expression-based risk score system can better predict both overall and recurrence-free survival in patients with small hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101497
                DO  - 10.18632/aging.101497
                SP  - 1627
                EP  - 1639
                PY  - 
                AB  - Growing evidence indicates that long non-coding RNAs (lncRNAs) may be potential biomarkers and therapeutic targets for many disease conditions, including cancer. In this study, we constructed a risk score system of three lncRNAs (LOC101927051, LINC00667 and NSUN5P2) for predicting the prognosis of small hepatocellular carcinoma (sHCC) (maximum tumor diameter ≤5 cm). The prognostic value of this sHCC risk model was confirmed in TCGA HCC samples (TNM stage I and II). Stratified survival analysis revealed that the suitable patient groups of the sHCC lncRNA-signature included HBV-infected and cirrhotic patients with better physical conditions yet lower levels of albumin and higher levels of alpha-fetoprotein preoperatively. Besides, Asian patients with no family history of HCC or history of alcohol consumption can be predicted more precisely. Molecular functional analysis indicated that PYK2 pathway was significantly enriched in the high-risk patients. Pathway enrichment analysis indicated that the two lncRNAs (LINC00667 and NSUN5P2) associated with poor prognosis were closely related to cell cycle. The nomogram based on the lncRNA-signature for RFS prediction in sHCC patients exhibited good performance in recurrence risk stratification. In conclusion, we identified a novel three-lncRNA-expression-based risk model for predicting the prognosis of sHCC.
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Caloric restriction effects on liver mTOR signaling are time-of-day dependent

Richa Tulsian, Nikkhil Velingkaar, Roman Kondratov,

https://doi.org/10.18632/aging.101498 pp 1640—1648

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Tulsian R, Velingkaar N, Kondratov R, . Caloric restriction effects on liver mTOR signaling are time-of-day dependent. . 10:1640-1648. https://doi.org/10.18632/aging.101498

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                TY  - JOUR
                AU  - Tulsian, Richa 
                AU  - Velingkaar, Nikkhil 
                AU  - Kondratov, Roman 
                TI  - Caloric restriction effects on liver mTOR signaling are time-of-day dependent
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101498
                DO  - 10.18632/aging.101498
                SP  - 1640
                EP  - 1648
                PY  - 
                AB  - The regulation of mechanistic target of rapamycin (mTOR) signaling contributes to the metabolic effects of a calorie restriction (CR) diet. We assayed the effect of CR on the activity of mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) in the liver of mice at six different times across the day. CR effects on mTORC1 and mTORC2 activities were time-of-day dependent. CR induced mTORC1 activity at one time, reduced at two times and has no effect during other times. CR induced mTORC2 activity at one time of the day and has no effects at other times. Circadian clocks are implemented in the regulation of mTOR signaling in mammals and mechanisms of CR. We assayed the effect of CR on mTOR signaling in the liver of mice deficient for circadian transcriptional regulators BMAL1 and CRYs. The CR induced suppression of mTORC1 activity was observed in both clock mutants, while up regulation of mTORC2 was observed in the liver of CRY deficient but not in the liver of BMAL1 deficient mice. Our finding revealed that CR has different time dependent effect on the activity of mTOR complexes 1 and 2 and suggest that circadian clock protein BMAL1 is involved in the up regulation of mTORC2 upon CR in mammals.
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Sodium fluoride induces splenocyte autophagy via the mammalian targets of rapamycin (mTOR) signaling pathway in growing mice

Ping Kuang, Huidan Deng, Huan Liu, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li, Xun Wang, Ling Zhao,

https://doi.org/10.18632/aging.101499 pp 1649—1665

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Kuang P, Deng H, Liu H, Cui H, Fang J, Zuo Z, Deng J, Li Y, Wang X, Zhao L, . Sodium fluoride induces splenocyte autophagy via the mammalian targets of rapamycin (mTOR) signaling pathway in growing mice. . 10:1649-1665. https://doi.org/10.18632/aging.101499

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                TY  - JOUR
                AU  - Kuang, Ping 
                AU  - Deng, Huidan 
                AU  - Liu, Huan 
                AU  - Cui, Hengmin 
                AU  - Fang, Jing 
                AU  - Zuo, Zhicai 
                AU  - Deng, Junliang 
                AU  - Li, Yinglun 
                AU  - Wang, Xun 
                AU  - Zhao, Ling 
                TI  - Sodium fluoride induces splenocyte autophagy via the mammalian targets of rapamycin (mTOR) signaling pathway in growing mice
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101499
                DO  - 10.18632/aging.101499
                SP  - 1649
                EP  - 1665
                PY  - 
                AB  - Fluoride is known to impair organism’s development and function via adverse effects, and autophagy plays a regulation role in human or animal health and disease. At present, there are no reports focused on fluoride-induced autophagy in the animal and human spleen. The objective of this study was to investigate sodium fluoride (NaF)-induced splenocyte autophagy and the potential mechanism via regulation of p-mTOR in growing mice by using the methods of transmission electron microscopy (TEM), immunohistochemistry (IHC), quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. A total of 240 ICR mice were equally allocated into four groups with intragastric administration of distilled water in the control group and 12, 24, 48 mg/kg NaF solution in the experimental groups for 42 days. Results revealed that NaF increased autophagosomes or autolysosomes in spleen. Simultaneously, the autophagy marker LC3 brown punctate staining was increased with NaF dosage increase. On the other hand, NaF caused inhibition of mTOR activity, which was characterized by down-regulation of PI3K, Akt and mTOR mRNA and protein expression levels. And the suppression of mTOR activity in turn resulted in the significantly increased of ULK1 and Atg13 expression levels. Concurrently, NaF increased the levels of mRNA and protein expression of autophagy markers LC3, Beclin1, Atg16L1, Atg12, Atg5 and decreased the mRNA and protein expression levels of p62. The above-mentioned findings verify that NaF induces autophagy via mTOR signaling pathway. The inhibition of mTOR activity and alteration of autophagy-related genes and proteins are the potential molecular mechanism of NaF-induced splenocyte autophagy.
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Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors HNRNPD and SRSF2

Eva Latorre, Roberta Torregrossa, Mark E. Wood, Matthew Whiteman, Lorna W. Harries,

https://doi.org/10.18632/aging.101500 pp 1666—1681

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Latorre E, Torregrossa R, Wood ME, Whiteman M, Harries LW, . Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors HNRNPD and SRSF2. . 10:1666-1681. https://doi.org/10.18632/aging.101500

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 TY - JOUR
 AU - Latorre, Eva 
 AU - Torregrossa, Roberta 
 AU - Wood, Mark E. 
 AU - Whiteman, Matthew 
 AU - Harries, Lorna W. 
 TI - Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors HNRNPD and SRSF2
 JO - 
 JA - 
 VL - 10
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101500
 DO - 10.18632/aging.101500
 SP - 1666
 EP - 1681
 PY - 
 AB - Cellular senescence is a key driver of ageing, influenced by age-related changes to the regulation of alternative splicing. Hydrogen sulfide (H2S) has similarly been described to influence senescence, but the pathways by which it accomplishes this are unclear.We assessed the effects of the slow release H2S donor Na-GYY4137 (100 µg/ml), and three novel mitochondria-targeted H2S donors AP39, AP123 and RT01 (10 ng/ml) on splicing factor expression, cell proliferation, apoptosis, DNA replication, DNA damage, telomere length and senescence-related secretory complex (SASP) expression in senescent primary human endothelial cells.All H2S donors produced up to a 50% drop in senescent cell load assessed at the biochemical and molecular level. Some changes were noted in the composition of senescence-related secretory complex (SASP); IL8 levels increased by 24% but proliferation was not re-established in the culture as a whole. Telomere length, apoptotic index and the extent of DNA damage were unaffected. Differential effects on splicing factor expression were observed depending on the intracellular targeting of the H2S donors. Na-GYY4137 produced a general 1.9 – 3.2-fold upregulation of splicing factor expression, whereas the mitochondria-targeted donors produced a specific 2.5 and 3.1-fold upregulation of SRSF2 and HNRNPD splicing factors only. Knockdown of SRSF2 or HNRNPD genes in treated cells rendered the cells non-responsive to H2S, and increased levels of senescence by up to 25% in untreated cells.Our data suggest that SRSF2 and HNRNPD may be implicated in endothelial cell senescence, and can be targeted by exogenous H2S. These molecules may have potential as moderators of splicing factor expression and senescence phenotypes.
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Global quantitative TPA-based proteomics of mouse brain structures reveals significant alterations in expression of proteins involved in neuronal plasticity during aging

Przemysław Duda, Olga Wójcicka, Jacek R. Wiśniewski, Dariusz Rakus,

https://doi.org/10.18632/aging.101501 pp 1682—1697

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Duda P, Wójcicka O, Wiśniewski JR, Rakus D, . Global quantitative TPA-based proteomics of mouse brain structures reveals significant alterations in expression of proteins involved in neuronal plasticity during aging. . 10:1682-1697. https://doi.org/10.18632/aging.101501

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                TY  - JOUR
                AU  - Duda, Przemysław 
                AU  - Wójcicka, Olga 
                AU  - Wiśniewski, Jacek R. 
                AU  - Rakus, Dariusz 
                TI  - Global quantitative TPA-based proteomics of mouse brain structures reveals significant alterations in expression of proteins involved in neuronal plasticity during aging
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101501
                DO  - 10.18632/aging.101501
                SP  - 1682
                EP  - 1697
                PY  - 
                AB  - Aging is believed to be the result of alterations of protein expression and accumulation of changes in biomolecules. Although there are numerous reports demonstrating changes in protein expression in brain during aging, only few of them describe global changes at the protein level. Here, we present the deepest quantitative proteomic analysis of three brain regions, hippocampus, cortex and cerebellum, in mice aged 1 or 12 months, using the total protein approach technique. In all the brain regions, both in young and middle-aged animals, we quantitatively measured over 5,200 proteins. We found that although the total protein expression in middle-aged brain structures is practically unaffected by aging, there are significant differences between young and middle-aged mice in the expression of some receptors and signaling cascade proteins proven to be significant for learning and memory formation. Our analysis demonstrates that the hippocampus is the most variable structure during natural aging and that the first symptoms of weakening of neuronal plasticity may be observed on protein level in middle-aged animals.
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Implementation of environmental enrichment after middle age promotes healthy aging

Travis McMurphy, Wei Huang, Nicholas J. Queen, Seemaab Ali, Kyle J. Widstrom, Xianglan Liu, Run Xiao, Jason J. Siu, Lei Cao,

https://doi.org/10.18632/aging.101502 pp 1698—1721

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McMurphy T, Huang W, Queen NJ, Ali S, Widstrom KJ, Liu X, Xiao R, Siu JJ, Cao L, . Implementation of environmental enrichment after middle age promotes healthy aging. . 10:1698-1721. https://doi.org/10.18632/aging.101502

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                TY  - JOUR
                AU  - McMurphy, Travis 
                AU  - Huang, Wei 
                AU  - Queen, Nicholas J. 
                AU  - Ali, Seemaab 
                AU  - Widstrom, Kyle J. 
                AU  - Liu, Xianglan 
                AU  - Xiao, Run 
                AU  - Siu, Jason J. 
                AU  - Cao, Lei 
                TI  - Implementation of environmental enrichment after middle age promotes healthy aging
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101502
                DO  - 10.18632/aging.101502
                SP  - 1698
                EP  - 1721
                PY  - 
                AB  - With increases in life expectancy, it is vital to understand the dynamics of aging, their interaction with lifestyle factors, and the connections to age-related disease processes. Our work on environmental enrichment (EE), a housing environment boosting mental health, has revealed a novel anticancer and anti-obesity phenotype mediated by a brain-fat axis: the hypothalamic-sympathoneural-adipocyte (HSA) axis in young animals. Here we investigated EE effects on healthspan and lifespan when initiated after middle age. Short-term EE for six weeks activated the HSA axis in 10-month-old mice. Long-term EE for twelve months reduced adiposity, improved glucose tolerance, decreased leptin levels, enhanced motor abilities, and inhibited anxiety. In addition to adipose remodeling, EE decreased age-related liver steatosis, reduced hepatic glucose production, and increased glucose uptake by liver and adipose tissue contributing to the improved glycemic control. The EE-induced liver modulation was associated with a suppression of protein kinase Cε. Moreover, EE down-regulated the expression of inflammatory genes in the brain, adipose, and liver. EE initiated at 18-month of age significantly improved glycemic control and showed a trend of positive impact on mean lifespan. These data suggest that EE induces metabolic and behavioral adaptations that are shared by factors known to increase healthspan and lifespan.
                ER  -

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Heme oxygenase-1 ameliorates oxidative stress-induced endothelial senescence via regulating endothelial nitric oxide synthase activation and coupling

Wenwei Luo, Yu Wang, Hanwei Yang, Chunmei Dai, Huiling Hong, Jingyan Li, Zhiping Liu, Zhen Guo, Xinyi Chen, Ping He, Ziqing Li, Fang Li, Jianmin Jiang, Peiqing Liu, Zhuoming Li,

https://doi.org/10.18632/aging.101506 pp 1722—1744

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Luo W, Wang Y, Yang H, Dai C, Hong H, Li J, Liu Z, Guo Z, Chen X, He P, Li Z, Li F, Jiang J, et al, . Heme oxygenase-1 ameliorates oxidative stress-induced endothelial senescence via regulating endothelial nitric oxide synthase activation and coupling. . 10:1722-1744. https://doi.org/10.18632/aging.101506

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                TY  - JOUR
                AU  - Luo, Wenwei 
                AU  - Wang, Yu 
                AU  - Yang, Hanwei 
                AU  - Dai, Chunmei 
                AU  - Hong, Huiling 
                AU  - Li, Jingyan 
                AU  - Liu, Zhiping 
                AU  - Guo, Zhen 
                AU  - Chen, Xinyi 
                AU  - He, Ping 
                AU  - Li, Ziqing 
                AU  - Li, Fang 
                AU  - Jiang, Jianmin 
                AU  - Liu, Peiqing 
                AU  - Li, Zhuoming 
                TI  - Heme oxygenase-1 ameliorates oxidative stress-induced endothelial senescence via regulating endothelial nitric oxide synthase activation and coupling
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101506
                DO  - 10.18632/aging.101506
                SP  - 1722
                EP  - 1744
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Luo, Wenwei 
                AU  - Wang, Yu 
                AU  - Yang, Hanwei 
                AU  - Dai, Chunmei 
                AU  - Hong, Huiling 
                AU  - Li, Jingyan 
                AU  - Liu, Zhiping 
                AU  - Guo, Zhen 
                AU  - Chen, Xinyi 
                AU  - He, Ping 
                AU  - Li, Ziqing 
                AU  - Li, Fang 
                AU  - Jiang, Jianmin 
                AU  - Liu, Peiqing 
                AU  - Li, Zhuoming 
                TI  - Heme oxygenase-1 ameliorates oxidative stress-induced endothelial senescence via regulating endothelial nitric oxide synthase activation and coupling
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101506
                DO  - 10.18632/aging.101506
                SP  - 1722
                EP  - 1744
                PY  - 
                AB  - Aim: Premature senescence of vascular endothelial cells is a leading cause of various cardiovascular diseases. Therapies targeting endothelial senescence would have important clinical implications. The present study was aimed to evaluate the potential of heme oxygenase-1 (HO-1) as a therapeutic target for endothelial senescence.Methods and Results: Upregulation of HO-1 by Hemin or adenovirus infection reversed H2O2-induced senescence in human umbilical vein endothelial cells (HUVECs); whereas depletion of HO-1 by siRNA or HO-1 inhibitor protoporphyrin IX zinc (II) (ZnPP) triggered HUVEC senescence. Mechanistically, overexpression of HO-1 enhanced the interaction between HO-1 and endothelial nitric oxide synthase (eNOS), and promoted the interaction between eNOS and its upstream kinase Akt, thus resulting in an enhancement of eNOS phosphorylation at Ser1177 and a subsequent increase of nitric oxide (NO) production. Moreover, HO-1 induction prevented the decrease of eNOS dimer/monomer ratio stimulated by H2O2 via its antioxidant properties. Contrarily, HO-1 silencing impaired eNOS phosphorylation and accelerated eNOS uncoupling. In vivo, Hemin treatment alleviated senescence of endothelial cells of the aorta from spontaneously hypertensive rats, through upregulating eNOS phosphorylation at Ser1177.Conclusions: HO-1 ameliorated endothelial senescence through enhancing eNOS activation and defending eNOS uncoupling, suggesting that HO-1 is a potential target for treating endothelial senescence.
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Cumulus cell-released tumor necrosis factor (TNF)-α promotes post-ovulatory aging of mouse oocytes

Qiao-Qiao Kong, Jia Wang, Bin Xiao, Fei-Hu Lin, Jiang Zhu, Guang-Yi Sun, Ming-Jiu Luo, Jing-He Tan,

https://doi.org/10.18632/aging.101507 pp 1745—1757

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Kong Q, Wang J, Xiao B, Lin F, Zhu J, Sun G, Luo M, Tan J, . Cumulus cell-released tumor necrosis factor (TNF)-α promotes post-ovulatory aging of mouse oocytes. . 10:1745-1757. https://doi.org/10.18632/aging.101507

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                TY  - JOUR
                AU  - Kong, Qiao-Qiao 
                AU  - Wang, Jia 
                AU  - Xiao, Bin 
                AU  - Lin, Fei-Hu 
                AU  - Zhu, Jiang 
                AU  - Sun, Guang-Yi 
                AU  - Luo, Ming-Jiu 
                AU  - Tan, Jing-He 
                TI  - Cumulus cell-released tumor necrosis factor (TNF)-α promotes post-ovulatory aging of mouse oocytes
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101507
                DO  - 10.18632/aging.101507
                SP  - 1745
                EP  - 1757
                PY  - 
                AB  - Although previous studies indicated that cumulus cells (CCs) accelerate oocyte aging by releasing soluble factors, the factors have yet to be characterized. While demonstrating that CCs promoted oocyte aging by releasing soluble Fas ligand (sFasL), our recent study suggested that CCs might secrete other factors to mediate oocyte aging as well. This study tested whether CCs accelerate oocyte aging by secreting tumor necrosis factor (TNF)-α. The results showed that mouse CCs undergoing apoptosis released soluble TNF-α (sTNF-α) during in vitro aging. While ethanol activation rates were higher, the maturation-promoting factor (MPF) activity was lower significantly after culture of cumulus-denuded oocytes (DOs) in medium conditioned with CCs for 36 h than in medium conditioned for 24 h. Aging mouse oocytes expressed TNF-receptor 1. The CCs released equal amounts of sTNF-α and sFasL during aging in vitro, and the TNF-α-knockdown CCs secreted less sFasL than the control CCs did. Treatment of DOs in vitro with sTNF-α significantly accelerated their aging. The aging-promoting effect of sTNF-α was significantly reduced in TNF-α-knocked-down CCs and in CCs from the TNF-α-knockout mice. It is concluded that mouse CCs accelerate oocyte aging by secreting sTNF-α as well as sFasL.
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Epigenetic clock for skin and blood cells applied to Hutchinson Gilford Progeria Syndrome and ex vivo studies

Steve Horvath, Junko Oshima, George M. Martin, Ake T. Lu, Austin Quach, Howard Cohen, Sarah Felton, Mieko Matsuyama, Donna Lowe, Sylwia Kabacik, James G. Wilson, Alex P. Reiner, Anna Maierhofer, Julia Flunkert, Abraham Aviv, Lifang Hou, Andrea A. Baccarelli, Yun Li, James D. Stewart, Eric A. Whitsel, Luigi Ferrucci, Shigemi Matsuyama, Kenneth Raj,

https://doi.org/10.18632/aging.101508 pp 1758—1775

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Horvath S, Oshima J, Martin GM, Lu AT, Quach A, Cohen H, Felton S, Matsuyama M, Lowe D, Kabacik S, Wilson JG, Reiner AP, Maierhofer A, et al, . Epigenetic clock for skin and blood cells applied to Hutchinson Gilford Progeria Syndrome and ex vivo studies. . 10:1758-1775. https://doi.org/10.18632/aging.101508

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Provider: 
 TY - JOUR
 AU - Horvath, Steve 
 AU - Oshima, Junko 
 AU - Martin, George M. 
 AU - Lu, Ake T. 
 AU - Quach, Austin 
 AU - Cohen, Howard 
 AU - Felton, Sarah 
 AU - Matsuyama, Mieko 
 AU - Lowe, Donna 
 AU - Kabacik, Sylwia 
 AU - Wilson, James G. 
 AU - Reiner, Alex P. 
 AU - Maierhofer, Anna 
 AU - Flunkert, Julia 
 AU - Aviv, Abraham 
 AU - Hou, Lifang 
 AU - Baccarelli, Andrea A. 
 AU - Li, Yun 
 AU - Stewart, James D. 
 AU - Whitsel, Eric A. 
 AU - Ferrucci, Luigi 
 AU - Matsuyama, Shigemi 
 AU - Raj, Kenneth 
 TI - Epigenetic clock for skin and blood cells applied to Hutchinson Gilford Progeria Syndrome and ex vivo studies
 JO - 
 JA - 
 VL - 10
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101508
 DO - 10.18632/aging.101508
 SP - 1758
 EP - 1775
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Horvath, Steve 
 AU - Oshima, Junko 
 AU - Martin, George M. 
 AU - Lu, Ake T. 
 AU - Quach, Austin 
 AU - Cohen, Howard 
 AU - Felton, Sarah 
 AU - Matsuyama, Mieko 
 AU - Lowe, Donna 
 AU - Kabacik, Sylwia 
 AU - Wilson, James G. 
 AU - Reiner, Alex P. 
 AU - Maierhofer, Anna 
 AU - Flunkert, Julia 
 AU - Aviv, Abraham 
 AU - Hou, Lifang 
 AU - Baccarelli, Andrea A. 
 AU - Li, Yun 
 AU - Stewart, James D. 
 AU - Whitsel, Eric A. 
 AU - Ferrucci, Luigi 
 AU - Matsuyama, Shigemi 
 AU - Raj, Kenneth 
 TI - Epigenetic clock for skin and blood cells applied to Hutchinson Gilford Progeria Syndrome and ex vivo studies
 JO - 
 JA - 
 VL - 10
 IS - 7
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101508
 DO - 10.18632/aging.101508
 SP - 1758
 EP - 1775
 PY - 
 AB - DNA methylation (DNAm)-based biomarkers of aging have been developed for many tissues and organs. However, these biomarkers have sub-optimal accuracy in fibroblasts and other cell types used in ex vivo studies. To address this challenge, we developed a novel and highly robust DNAm age estimator (based on 391 CpGs) for human fibroblasts, keratinocytes, buccal cells, endothelial cells, lymphoblastoid cells, skin, blood, and saliva samples. High age correlations can also be observed in sorted neurons, glia, brain, liver, and even bone samples. Gestational age correlates with DNAm age in cord blood. When used on fibroblasts from Hutchinson Gilford Progeria Syndrome patients, this age estimator (referred to as the skin &amp; blood clock) uncovered an epigenetic age acceleration with a magnitude that is below the sensitivity levels of other DNAm-based biomarkers. Furthermore, this highly sensitive age estimator accurately tracked the dynamic aging of cells cultured ex vivo and revealed that their proliferation is accompanied by a steady increase in epigenetic age. The skin &amp; blood clock predicts lifespan and it relates to many age-related conditions. Overall, this biomarker is expected to become useful for forensic applications (e.g. blood or buccal swabs) and for a quantitative ex vivo human cell aging assay.
 ER -

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Human methionine synthase A2756G polymorphism increases susceptibility to prostate cancer

Hong-Bao Shao, Kewei Ren, Sheng-Lin Gao, Jian-Gang Zou, Yuan-Yuan Mi, Li-Feng Zhang, Li Zuo, Atsushi Okada, Takahiro Yasui,

https://doi.org/10.18632/aging.101509 pp 1776—1788

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Shao H, Ren K, Gao S, Zou J, Mi Y, Zhang L, Zuo L, Okada A, Yasui T, . Human methionine synthase A2756G polymorphism increases susceptibility to prostate cancer. . 10:1776-1788. https://doi.org/10.18632/aging.101509

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                TY  - JOUR
                AU  - Shao, Hong-Bao 
                AU  - Ren, Kewei 
                AU  - Gao, Sheng-Lin 
                AU  - Zou, Jian-Gang 
                AU  - Mi, Yuan-Yuan 
                AU  - Zhang, Li-Feng 
                AU  - Zuo, Li 
                AU  - Okada, Atsushi 
                AU  - Yasui, Takahiro 
                TI  - Human methionine synthase A2756G polymorphism increases susceptibility to prostate cancer
                JO  - 
                JA  - 
                VL  - 10
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101509
                DO  - 10.18632/aging.101509
                SP  - 1776
                EP  - 1788
                PY  - 
                AB  - Background/Aims: Previous results on the association between MTR gene A2756G polymorphism and PCa risk are inconclusive.Methods: We used odds ratios (ORs) with corresponding 95% confidence intervals (95% CIs) to evaluate the correlation between MTR A2756G polymorphism and risk of PCa in meta-analysis. Serum expression of MTR was detected by ELISA and in-silico tools were utilized to assess this variant.Results: Our study included 2,921 PCa patients and 3,095 control subjects. The results indicated that the MTR A2756G polymorphism is linked with an increased risk of PCa using three genetic models (G-allele vs. A-allele: OR = 1.16, 95%CI = 1.04 - 1.30; GA vs. AA: OR = 1.17, 95%CI = 1.02 - 1.33; GG+GA vs. AA: OR = 1.18, 95%CI = 1.04 - 1.34). Stratified analysis produced similar results. A significant association was also indicated in advanced PCa from the meta-analysis. Finally, our experiments showed evidence that serum MTR levels in PCa patients with AA genotypes were statistically higher than in those with GG/GA genotypes.Conclusions: Our present study suggests that the MTR A2756G polymorphism may contribute to the risk of developing PCa, particularly in Asian and hospital-based studies. Moreover, serum MTR might be utilized in diagnosis of PCa.
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Volume 10, Issue 7

About the Cover

Editorials

Oleg Podgorny, Natalia Peunova, Grigori Enikolopov,

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Erin K. Crowley, Yvonne M. Nolan, Aideen M. Sullivan,

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Laura Camacho, Amaia Zabala-Letona, Arkaitz Carracedo,

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Claude Alain, Linda Garami, Kristina C. Backer,

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Research Papers

Emma Anderson, Alice Cochrane, Jean Golding, Stephen Nowicki,

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Shun-Feng Cheng, Xun-Si Qin, Ze-Li Han, Xiao-Feng Sun, Yan-Ni Feng, Fan Yang, Wei Ge, Lan Li, Yong Zhao, Massimo De Felici, Shu-Hua Zou, Yi Zhou, Wei Shen,

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Nicola Alessio, Antonietta Stellavato, Tiziana Squillaro, Stefania Del Gaudio, Giovanni Di Bernardo, Gianfranco Peluso, Mario De Rosa, Chiara Schiraldi, Umberto Galderisi,

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Qiu-Xia Liang, Yi-Hua Lin, Chun-Hui Zhang, Hong-Mei Sun, Liang Zhou, Heide Schatten, Qing-Yuan Sun, Wei-Ping Qian,

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Hao Gu, Dong Liu, Xi Zeng, Liu-Sheng Peng, Yue Yuan, Zhi-Fu Chen, Quan-Ming Zou, Yun Shi,

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Byuri Angela Cho, Seong-Keun Yoo, Jeong-Sun Seo,

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Jingxian Gu, Xing Zhang, Runchen Miao, Xiaohua Ma, Xiaohong Xiang, Yunong Fu, Chang Liu, Wenquan Niu, Kai Qu,

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Richa Tulsian, Nikkhil Velingkaar, Roman Kondratov,

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Ping Kuang, Huidan Deng, Huan Liu, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Yinglun Li, Xun Wang, Ling Zhao,

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Eva Latorre, Roberta Torregrossa, Mark E. Wood, Matthew Whiteman, Lorna W. Harries,

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Przemysław Duda, Olga Wójcicka, Jacek R. Wiśniewski, Dariusz Rakus,

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Travis McMurphy, Wei Huang, Nicholas J. Queen, Seemaab Ali, Kyle J. Widstrom, Xianglan Liu, Run Xiao, Jason J. Siu, Lei Cao,

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Wenwei Luo, Yu Wang, Hanwei Yang, Chunmei Dai, Huiling Hong, Jingyan Li, Zhiping Liu, Zhen Guo, Xinyi Chen, Ping He, Ziqing Li, Fang Li, Jianmin Jiang, Peiqing Liu, Zhuoming Li,

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Qiao-Qiao Kong, Jia Wang, Bin Xiao, Fei-Hu Lin, Jiang Zhu, Guang-Yi Sun, Ming-Jiu Luo, Jing-He Tan,

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Hong-Bao Shao, Kewei Ren, Sheng-Lin Gao, Jian-Gang Zou, Yuan-Yuan Mi, Li-Feng Zhang, Li Zuo, Atsushi Okada, Takahiro Yasui,