Volume 11, Issue 13

Cheng D, Tang Y, Li H, Li Y, Sang H, . Nighttime blood pressure decline as a predictor of renal injury in patients with hypertension: a population-based cohort study. . 11:4310-4322. https://doi.org/10.18632/aging.101873

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                TY  - JOUR
                AU  - Cheng, Dong 
                AU  - Tang, Yi 
                AU  - Li, Haiyu 
                AU  - Li, Yunpeng 
                AU  - Sang, Haiqiang 
                TI  - Nighttime blood pressure decline as a predictor of renal injury in patients with hypertension: a population-based cohort study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101873
                DO  - 10.18632/aging.101873
                SP  - 4310
                EP  - 4322
                PY  - 
                AB  - We explored whether the nighttime blood pressure (BP) decline predicts renal function decline in a population-based cohort with primary hypertension. We measured the baseline ambulatory BP and glomerular filtration rate (GFR) in a cohort of 1,042 primary hypertensive patients. We repeated the GFR measurements and calculated the rate of GFR decline after a median follow-up of 5.8 years. The estimated GFR (eGFR) declined by &#x2212;0.23 to &#x2212;0.20 mL/min per year as the nighttime systolic BP (SBP), diastolic BP (DBP), and mean BP decline rates increased by 1% (P &lt; 0.001). In the fully adjusted model, the nighttime SBP, DBP, and mean BP were all related to a steeper rate of eGFR decline by &#x2212;0.25 to &#x2212;0.22 mL/min per 1% increase. The adjusted multivariable results indicated that the odds of an eGFR decline were reduced by 46% when the nighttime SBP decline rate increased by 1% (OR= 0.54, 95% CI: 0.46&#x2013;0.62). The restricted cubic spline model indicated a non-linear dose-response relationship with the nighttime SBP, DBP, and mean BP. Nighttime BP may be an important biomarker of renal function injury in hypertensive patients.
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HMGB1 and Caveolin-1 related to RPE cell senescence in age-related macular degeneration

Shuo Sun, Bincui Cai, Yao Li, Wenqi Su, Xuzheng Zhao, Boteng Gong, Zhiqing Li, Xiaomin Zhang, Yalin Wu, Chao Chen, Stephen H. Tsang, Jin Yang, Xiaorong Li,

https://doi.org/10.18632/aging.102039 pp 4323—4337

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Sun S, Cai B, Li Y, Su W, Zhao X, Gong B, Li Z, Zhang X, Wu Y, Chen C, Tsang SH, Yang J, Li X, . HMGB1 and Caveolin-1 related to RPE cell senescence in age-related macular degeneration. . 11:4323-4337. https://doi.org/10.18632/aging.102039

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                TY  - JOUR
                AU  - Sun, Shuo 
                AU  - Cai, Bincui 
                AU  - Li, Yao 
                AU  - Su, Wenqi 
                AU  - Zhao, Xuzheng 
                AU  - Gong, Boteng 
                AU  - Li, Zhiqing 
                AU  - Zhang, Xiaomin 
                AU  - Wu, Yalin 
                AU  - Chen, Chao 
                AU  - Tsang, Stephen H. 
                AU  - Yang, Jin 
                AU  - Li, Xiaorong 
                TI  - HMGB1 and Caveolin-1 related to RPE cell senescence in age-related macular degeneration
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102039
                DO  - 10.18632/aging.102039
                SP  - 4323
                EP  - 4337
                PY  - 
                AB  - Accumulation of lipofuscin in the retinal pigment epithelium (RPE) is considered a major cause of RPE dysfunction and senescence in age-related macular degeneration (AMD), and N-retinylidene-N-retinylethanolamine (A2E) is the main fluorophore identified in lipofuscin from aged human eyes. Here, human-induced pluripotent stem cell (iPSC)-RPE was generated from healthy individuals to reveal proteomic changes associated with A2E-related RPE cell senescence. A novel RPE cell senescence-related protein, high-mobility group box 1 (HMGB1), was identified based on proteomic mass spectrometry measurements on iPSC-RPE with A2E treatment. Furthermore, HMGB1 upregulated Caveolin-1, which also was related RPE cell senescence. To investigate whether changes in HMGB1 and Caveolin-1 expression under A2E exposure contribute to RPE cell senescence, human ARPE-19 cells were stimulated with A2E; expression of HMGB1, Caveolin-1, tight junction proteins and senescent phenotypes were verified. HMGB1 inhibition alleviated A2E induced cell senescence. Migration of RPE cells was evaluated. Notably, A2E less than or equal to 10&#x3BC;M induced both HMGB1 and Caveolin-1 protein upregulation and HMGB1 translocation, while Caveolin-1 expression was downregulated when there was more than 10&#x3BC;M A2E. Our data indicate that A2E-induced upregulation of HMGB1&#x3001;Caveolin-1 and HMGB1 release may relate to RPE cell senescence and play a role in the pathogenesis of AMD.
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Targeting HMGB1 by ethyl pyruvate ameliorates systemic lupus erythematosus and reverses the senescent phenotype of bone marrow-mesenchymal stem cells

Juan Ji, Ting Fu, Chen Dong, Wenyan Zhu, Junling Yang, Xiaoli Kong, Zhongyuan Zhang, Yanfeng Bao, Rui Zhao, Xinyu Ge, Xiaoqi Sha, Zhimin Lu, Jing Li, Zhifeng Gu,

https://doi.org/10.18632/aging.102052 pp 4338—4353

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Ji J, Fu T, Dong C, Zhu W, Yang J, Kong X, Zhang Z, Bao Y, Zhao R, Ge X, Sha X, Lu Z, Li J, et al, . Targeting HMGB1 by ethyl pyruvate ameliorates systemic lupus erythematosus and reverses the senescent phenotype of bone marrow-mesenchymal stem cells. . 11:4338-4353. https://doi.org/10.18632/aging.102052

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                TY  - JOUR
                AU  - Ji, Juan 
                AU  - Fu, Ting 
                AU  - Dong, Chen 
                AU  - Zhu, Wenyan 
                AU  - Yang, Junling 
                AU  - Kong, Xiaoli 
                AU  - Zhang, Zhongyuan 
                AU  - Bao, Yanfeng 
                AU  - Zhao, Rui 
                AU  - Ge, Xinyu 
                AU  - Sha, Xiaoqi 
                AU  - Lu, Zhimin 
                AU  - Li, Jing 
                AU  - Gu, Zhifeng 
                TI  - Targeting HMGB1 by ethyl pyruvate ameliorates systemic lupus erythematosus and reverses the senescent phenotype of bone marrow-mesenchymal stem cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102052
                DO  - 10.18632/aging.102052
                SP  - 4338
                EP  - 4353
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ji, Juan 
                AU  - Fu, Ting 
                AU  - Dong, Chen 
                AU  - Zhu, Wenyan 
                AU  - Yang, Junling 
                AU  - Kong, Xiaoli 
                AU  - Zhang, Zhongyuan 
                AU  - Bao, Yanfeng 
                AU  - Zhao, Rui 
                AU  - Ge, Xinyu 
                AU  - Sha, Xiaoqi 
                AU  - Lu, Zhimin 
                AU  - Li, Jing 
                AU  - Gu, Zhifeng 
                TI  - Targeting HMGB1 by ethyl pyruvate ameliorates systemic lupus erythematosus and reverses the senescent phenotype of bone marrow-mesenchymal stem cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102052
                DO  - 10.18632/aging.102052
                SP  - 4338
                EP  - 4353
                PY  - 
                AB  - Systemic lupus erythematosus (SLE) is a chronic autoimmune disease involving multiple organs and systems. Mesenchymal stem cells (MSCs) from SLE patients have demonstrated defects such as impaired growth, senescence phenotype and immunomodulatory functions. Some studies have suggested the close connection between inflammation microenvironment and cellular senescence. In the current study, we detected cytokines levels in bone marrow supernatant by the quantitative proteomics analysis, and found the expression of HMGB1 was remarkably increased in bone marrow from SLE patients. Senescence associated-&#x3B2;-galactosidase (SA-&#x3B2;-gal) staining, F-actin staining and flow cytometry were used to detect the senescence of cells. After stimulation of HMGB1 in normal MSCs, the ratio of SA-&#x3B2;-gal positive in BM-MSCs was increased, the organization of cytoskeleton was disordered, and TLR4-NF-&#x3BA;B signaling was activated. Finally, Ethyl pyruvate (EP) (40 mg/kg and 100 mg/kg, three times a week), a high security HMGB1 inhibitor, was injected intraperitoneally to treat MRL/lpr mice for 8 weeks. We demonstrated that EP alleviated the clinical aspects of lupus nephritis and prolonged survival of MRL/lpr mice. In the meantime, EP reversed the senescent phenotype of BM-MSCs from MRL/lpr mice. HMGB1 could be a promising target in SLE patients, and might be one of the reasons of recurrence after MSCs transplantation.
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Ammonia induces calpain-dependent cleavage of CRMP-2 during neurite degeneration in primary cultured neurons

Zhenbin Cai, Xiaonan Zhu, Guowei Zhang, Fengming Wu, Hongsheng Lin, Minghui Tan,

https://doi.org/10.18632/aging.102053 pp 4354—4366

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Cai Z, Zhu X, Zhang G, Wu F, Lin H, Tan M, . Ammonia induces calpain-dependent cleavage of CRMP-2 during neurite degeneration in primary cultured neurons. . 11:4354-4366. https://doi.org/10.18632/aging.102053

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                TY  - JOUR
                AU  - Cai, Zhenbin 
                AU  - Zhu, Xiaonan 
                AU  - Zhang, Guowei 
                AU  - Wu, Fengming 
                AU  - Lin, Hongsheng 
                AU  - Tan, Minghui 
                TI  - Ammonia induces calpain-dependent cleavage of CRMP-2 during neurite degeneration in primary cultured neurons
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102053
                DO  - 10.18632/aging.102053
                SP  - 4354
                EP  - 4366
                PY  - 
                AB  - Hyperammonemia in the CNS induces irreversible damages to neurons due to ultimate cell loss. Neurite degeneration, a primary event that leads to neuronal cell death, remains less elucidated especially in hyperammonemia circumstances. Here, we found that the administration of ammonia induced neurite degeneration in cultured cerebellar granule neurons. The resulting altered neuronal morphology, rupture of neurites, and disassembly of the cytoskeleton led to cell death. Calcein and Fluo-4 staining revealed that ammonia induced intracellular calcium dysregulation. Subsequently activated calpain cleaved CRMP-2, a microtubule assembly protein. Pharmacologically inhibition of calpain, but not caspases or GSK-3, suppressed the cleavage of CRMP-2 and reversed neurite degeneration under ammonia treatment. Exposure to ammonia decreased whereas inhibition of calpain restored the amplitude and frequency of miniature excitatory postsynaptic currents. These data suggest a mechanism by which elevated ammonia level may induce neuronal dysfunction via abnormal calcium influx and calpain-dependent CRMP-2 cleavage, leading to abnormal synaptic transmission, cytoskeletal collapse, and neurite degeneration.
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Age-related changes in B cell metabolism

Raj K. Kurupati, Larissa H. Haut, Kenneth E. Schmader, Hildegund CJ. Ertl,

https://doi.org/10.18632/aging.102058 pp 4367—4381

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Kurupati RK, Haut LH, Schmader KE, Ertl HC, . Age-related changes in B cell metabolism. . 11:4367-4381. https://doi.org/10.18632/aging.102058

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                TY  - JOUR
                AU  - Kurupati, Raj K.
                AU  - Haut, Larissa H.
                AU  - Schmader, Kenneth E.
                AU  - Ertl, Hildegund CJ.
                TI  - Age-related changes in B cell metabolism
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102058
                DO  - 10.18632/aging.102058
                SP  - 4367
                EP  - 4381
                PY  - 
                AB  - Antibody responses to vaccinations or infections decline upon aging. In this study we tested if metabolic changes in B cells may contribute to attenuation of responses to influenza vaccination in aged humans. Our data show that aging affects mitochondrial functions in B cells leading to increases in mitochondrial reactive oxygen species (MROS) and mitochondrial mass (MM) in some aged B cell subsets and decreases in expression levels of Sirtuin 1 (SIRT1), Forkhead box protein (FOX)O1 and carnitine palmitoyltransferase 1 (CPT-1). Seahorse analyses showed minor defects in glycolysis in the aged B cells after activation but a strong reduction in oxidative phosphorylation. The analyses of the transcriptome revealed further pronounced defects in one-carbon metabolism, a pathway that is essential for amino acid and nucleotide metabolism. Overall our data support the notion that the declining ability of aged B cells to increase their metabolism following activation contributes to the weakened antibody responses of the elderly.
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Complement component C5a induces aberrant epigenetic modifications in renal tubular epithelial cells accelerating senescence by Wnt4/βcatenin signaling after ischemia/reperfusion injury

Giuseppe Castellano, Rossana Franzin, Fabio Sallustio, Alessandra Stasi, Barbara Banelli, Massimo Romani, Giuseppe De Palma, Giuseppe Lucarelli, Chiara Divella, Michele Battaglia, Antonio Crovace, Francesco Staffieri, Giuseppe Grandaliano, Giovanni Stallone, Pasquale Ditonno, Paolo Cravedi, Vincenzo Cantaluppi, Loreto Gesualdo,

https://doi.org/10.18632/aging.102059 pp 4382—4406

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Castellano G, Franzin R, Sallustio F, Stasi A, Banelli B, Romani M, De Palma G, Lucarelli G, Divella C, Battaglia M, Crovace A, Staffieri F, Grandaliano G, et al, . Complement component C5a induces aberrant epigenetic modifications in renal tubular epithelial cells accelerating senescence by Wnt4/βcatenin signaling after ischemia/reperfusion injury. . 11:4382-4406. https://doi.org/10.18632/aging.102059

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                TY  - JOUR
                AU  - Castellano, Giuseppe 
                AU  - Franzin, Rossana 
                AU  - Sallustio, Fabio 
                AU  - Stasi, Alessandra 
                AU  - Banelli, Barbara 
                AU  - Romani, Massimo 
                AU  - De Palma, Giuseppe 
                AU  - Lucarelli, Giuseppe 
                AU  - Divella, Chiara 
                AU  - Battaglia, Michele 
                AU  - Crovace, Antonio 
                AU  - Staffieri, Francesco 
                AU  - Grandaliano, Giuseppe 
                AU  - Stallone, Giovanni 
                AU  - Ditonno, Pasquale 
                AU  - Cravedi, Paolo 
                AU  - Cantaluppi, Vincenzo 
                AU  - Gesualdo, Loreto 
                TI  - Complement component C5a induces aberrant epigenetic modifications in renal tubular epithelial cells accelerating senescence by Wnt4/βcatenin signaling after ischemia/reperfusion injury
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102059
                DO  - 10.18632/aging.102059
                SP  - 4382
                EP  - 4406
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Castellano, Giuseppe 
                AU  - Franzin, Rossana 
                AU  - Sallustio, Fabio 
                AU  - Stasi, Alessandra 
                AU  - Banelli, Barbara 
                AU  - Romani, Massimo 
                AU  - De Palma, Giuseppe 
                AU  - Lucarelli, Giuseppe 
                AU  - Divella, Chiara 
                AU  - Battaglia, Michele 
                AU  - Crovace, Antonio 
                AU  - Staffieri, Francesco 
                AU  - Grandaliano, Giuseppe 
                AU  - Stallone, Giovanni 
                AU  - Ditonno, Pasquale 
                AU  - Cravedi, Paolo 
                AU  - Cantaluppi, Vincenzo 
                AU  - Gesualdo, Loreto 
                TI  - Complement component C5a induces aberrant epigenetic modifications in renal tubular epithelial cells accelerating senescence by Wnt4/βcatenin signaling after ischemia/reperfusion injury
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102059
                DO  - 10.18632/aging.102059
                SP  - 4382
                EP  - 4406
                PY  - 
                AB  - Epigenetic mechanisms, such as DNA methylation, affect tubular maladaptive response after Acute Kidney Injury (AKI) and accelerate renal aging. Upon ischemia/reperfusion (I/R) injury, Complement activation leads to C5a release that mediates damage; however, little is known about the effect of C5a-C5a Receptor (C5aR) interaction in Renal Tubular Epithelial Cells (RTEC).Through a whole-genome DNA methylation analysis in cultured RTEC, we found that C5a induced aberrant methylation, particularly in regions involved in cell cycle control, DNA damage and Wnt signaling. The most represented genes were BCL9, CYP1B1 and CDK6. C5a stimulation of RTEC led to up-regulation of SA-&#x3B2; Gal and cell cycle arrest markers such as p53 and p21. C5a increased also IL-6, MCP-1 and CTGF gene expression, consistent with SASP development. In accordance, in a swine model of renal I/R injury, we found the increased expression of Wnt4 and &#x3B2;catenin correlating with SA-&#x3B2; Gal, p21, p16 and IL-6 positivity. Administration of Complement Inhibitor (C1-Inh), antagonized SASP by reducing SA-&#x3B2; Gal, p21, p16, IL-6 and abrogating Wnt4/&#x3B2;catenin activation.Thus, C5a affects the DNA methylation of genes involved in tubular senescence. Targeting epigenetic programs and Complement may offer novels strategies to protect tubular cells from accelerated aging and to counteract progression to Chronic Kidney Disease
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HNRNPA1-mediated 3′ UTR length changes of HN1 contributes to cancer- and senescence-associated phenotypes

Qi Jia, Hongbo Nie, Peng Yu, Baiyun Xie, Chenji Wang, Fu Yang, Gang Wei, Ting Ni,

https://doi.org/10.18632/aging.102060 pp 4407—4437

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Jia Q, Nie H, Yu P, Xie B, Wang C, Yang F, Wei G, Ni T, . HNRNPA1-mediated 3′ UTR length changes of HN1 contributes to cancer- and senescence-associated phenotypes. . 11:4407-4437. https://doi.org/10.18632/aging.102060

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 TY - JOUR
 AU - Jia, Qi 
 AU - Nie, Hongbo 
 AU - Yu, Peng 
 AU - Xie, Baiyun 
 AU - Wang, Chenji 
 AU - Yang, Fu 
 AU - Wei, Gang 
 AU - Ni, Ting 
 TI - HNRNPA1-mediated 3′ UTR length changes of HN1 contributes to cancer- and senescence-associated phenotypes
 JO - 
 JA - 
 VL - 11
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102060
 DO - 10.18632/aging.102060
 SP - 4407
 EP - 4437
 PY - 
 AB - Cellular senescence has been regarded as a mechanism of tumor suppression. Studying the regulation of gene expression at various levels in cell senescence will shed light on cancer therapy. Alternative polyadenylation (APA) regulates gene expression by altering 3&#x2032; untranslated regions (3&#x2032; UTR) and plays important roles in diverse biological processes. However, whether APA of a specific gene functions in both cancer and senescence remains unclear. Here, we discovered that 3&#x2032; UTR of HN1 (or JPT1) showed shortening in cancers and lengthening in senescence, correlated well with its high expression in cancer cells and low expression in senescent cells, respectively. HN1 transcripts with longer 3&#x2032; UTR were less stable and produced less protein. Down-regulation of HN1 induced senescence-associated phenotypes in both normal and cancer cells. Patients with higher HN1 expression had lower survival rates in various carcinomas. Interestingly, down-regulating the splicing factor HNRNPA1 induced 3&#x2032; UTR lengthening of HN1 and senescence-associated phenotypes, which could be partially reversed by overexpressing HN1. Together, we revealed for the first time that HNRNPA1-mediated APA of HN1 contributed to cancer- and senescence-related phenotypes. Given senescence is a cancer prevention mechanism, our discovery indicates the HNRNPA1-HN1 axis as a potential target for cancer treatment.
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Fasting blood glucose level and hypertension risk in aging benign prostatic hyperplasia patients

Hao Zi, Xue-Jun Wang, Ming-Juan Zhao, Qiao Huang, Xing-Huan Wang, Xian-Tao Zeng,

https://doi.org/10.18632/aging.102061 pp 4438—4445

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Zi H, Wang X, Zhao M, Huang Q, Wang X, Zeng X, . Fasting blood glucose level and hypertension risk in aging benign prostatic hyperplasia patients. . 11:4438-4445. https://doi.org/10.18632/aging.102061

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                TY  - JOUR
                AU  - Zi, Hao 
                AU  - Wang, Xue-Jun 
                AU  - Zhao, Ming-Juan 
                AU  - Huang, Qiao 
                AU  - Wang, Xing-Huan 
                AU  - Zeng, Xian-Tao 
                TI  - Fasting blood glucose level and hypertension risk in aging benign prostatic hyperplasia patients
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102061
                DO  - 10.18632/aging.102061
                SP  - 4438
                EP  - 4445
                PY  - 
                AB  - Evidence suggests there maybe an association among abnormal fasting blood glucose, hypertension and benign prostatic hyperplasia. In this study, we investigated whether abnormal fasting blood glucose correlates with hypertension in aging benign prostatic hyperplasia patients. Ultimately, 612 benign prostatic hyperplasia patients, including 230 hypertensive patients and 382 normotensive patients, were included. Univariate and multivariate logistic regression analyses were used to evaluate the associations. The results indicated that neither impaired fasting glucose/high risk of type 2 diabetes mellitus nor high risk of type 2 diabetes mellitus were associated with an increased risk of hypertension. When patients were stratified based on the severity of their hypertension, similar results were obtained (all P&gt; 0.05). After adjusting for confounding factors, the nonsignificant tendencies for high risk of type 2 diabetes mellitus and impaired fasting glucose/high risk of type 2 diabetes mellitus to associate with hypertension persisted (all P&gt; 0.05). Unlike earlier studies, the present study suggests that the level of fasting blood glucose may not be significantly related to hypertension in aging patients with benign prostatic hyperplasia.
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Prognostic value of serum lactate kinetics in critically ill patients with cirrhosis and acute-on-chronic liver failure: a multicenter study

Feng Gao, Xie-lin Huang, Meng-Xing Cai, Miao-tong Lin, Bin-feng Wang, Wei Wu, Zhi-Ming Huang,

https://doi.org/10.18632/aging.102062 pp 4446—4462

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Gao F, Huang X, Cai M, Lin M, Wang B, Wu W, Huang Z, . Prognostic value of serum lactate kinetics in critically ill patients with cirrhosis and acute-on-chronic liver failure: a multicenter study. . 11:4446-4462. https://doi.org/10.18632/aging.102062

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                TY  - JOUR
                AU  - Gao, Feng 
                AU  - Huang, Xie-lin 
                AU  - Cai, Meng-Xing 
                AU  - Lin, Miao-tong 
                AU  - Wang, Bin-feng 
                AU  - Wu, Wei 
                AU  - Huang, Zhi-Ming 
                TI  - Prognostic value of serum lactate kinetics in critically ill patients with cirrhosis and acute-on-chronic liver failure: a multicenter study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102062
                DO  - 10.18632/aging.102062
                SP  - 4446
                EP  - 4462
                PY  - 
                AB  - Lactate clearance (&#x394;24Lac) was reported to be inversely associated with mortality in critically ill patients. The aim of our study was to assess the value of &#x394;24Lac for the prognosis of critically ill patients with cirrhosis and acute-on-chronic liver failure (ACLF). We analysed 954 cirrhotic patients with hyperlactatemia admitted to intensive care units (ICUs) in the United States and eastern China. The patients were followed up for at least 1 year. In the unadjusted model, we observed a 15% decrease in hospital mortality with each 10% increase in &#x394;24Lac. In the fully adjusted model, the relationship between the risk of death and &#x394;24Lac remained statistically significant (hospital mortality: odds ratio [OR] 0.84, 95% confidence interval [CI]: 0.78- 0.90, p &lt; 0.001; 90-day mortality: hazard ratio [HR] 0.94, 95%CI 0.92- 0.97, p &lt; 0.001; for &#x394;24Lac per 10% increase). Similar results were found in patients with ACLF. We developed a &#x394;24Lac-adjusted score (LiFe-&#x394;24Lac), which performed significantly better in the area under the receiver operating characteristic curves (AUROCs) than the original LiFe score for predicting mortality. Lactate clearance is an independent predictor of death, and the LiFe-&#x394;24Lac score is a practical tool for stratifying the risk of death.
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Let-7f-5p suppresses Th17 differentiation via targeting STAT3 in multiple sclerosis

Zhi-Hui Li, Yi-Fei Wang, Dan-Dan He, Xue-Mei Zhang, Ying-Lian Zhou, Hui Yue, Shan Huang, Zheng Fu, Ling-Yu Zhang, Zhu-Qing Mao, Shuang Li, Chen-Yu Zhang, Xi Chen, Jin Fu,

https://doi.org/10.18632/aging.102093 pp 4463—4477

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Li Z, Wang Y, He D, Zhang X, Zhou Y, Yue H, Huang S, Fu Z, Zhang L, Mao Z, Li S, Zhang C, Chen X, et al, . Let-7f-5p suppresses Th17 differentiation via targeting STAT3 in multiple sclerosis. . 11:4463-4477. https://doi.org/10.18632/aging.102093

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                TY  - JOUR
                AU  - Li, Zhi-Hui 
                AU  - Wang, Yi-Fei 
                AU  - He, Dan-Dan 
                AU  - Zhang, Xue-Mei 
                AU  - Zhou, Ying-Lian 
                AU  - Yue, Hui 
                AU  - Huang, Shan 
                AU  - Fu, Zheng 
                AU  - Zhang, Ling-Yu 
                AU  - Mao, Zhu-Qing 
                AU  - Li, Shuang 
                AU  - Zhang, Chen-Yu 
                AU  - Chen, Xi 
                AU  - Fu, Jin 
                TI  - Let-7f-5p suppresses Th17 differentiation via targeting STAT3 in multiple sclerosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102093
                DO  - 10.18632/aging.102093
                SP  - 4463
                EP  - 4477
                PY  - 
                AB  - T helper 17 (Th17) cells are regarded as key factors in the pathogenesis of multiple sclerosis (MS). Although the involvement of certain microRNAs (miRNAs) in the development of MS has been reported, their roles in Th17 cell differentiation and MS pathogenesis remain elusive. In this study, we identified that let-7f-5p expression is significantly downregulated in CD4+ T cells from MS patients and during the process of Th17 differentiation. The overexpression of let-7f-5p suppressed Th17 differentiation, whereas the knockdown of let-7f-5p expression enhanced this progress. We then explored the molecular mechanism through which let-7f-5p suppressed Th17 differentiation and identified signal transducer and activator of transcription 3 (STAT3), a pivotal transcription factor of Th17 cells, as a direct target of let-7f-5p. In contrast to the downregulated expression of let-7f-5p, STAT3 and p-STAT3 protein levels were dramatically upregulated and inversely correlated with let-7f-5p in peripheral blood CD4+ T cells from MS patients. In conclusion, let-7f-5p functions as a potential inhibitor of Th17 differentiation in the pathogenesis of MS by targeting STAT3 and may serve as a new therapeutic target.
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Integrated tumor stromal features of hepatocellular carcinoma reveals two distinct subtypes with prognostic/predictive significance

Wei Li, Jun Han, Kefei Yuan, Hong Wu,

https://doi.org/10.18632/aging.102064 pp 4478—4509

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Li W, Han J, Yuan K, Wu H, . Integrated tumor stromal features of hepatocellular carcinoma reveals two distinct subtypes with prognostic/predictive significance. . 11:4478-4509. https://doi.org/10.18632/aging.102064

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                TY  - JOUR
                AU  - Li, Wei 
                AU  - Han, Jun 
                AU  - Yuan, Kefei 
                AU  - Wu, Hong 
                TI  - Integrated tumor stromal features of hepatocellular carcinoma reveals two distinct subtypes with prognostic/predictive significance
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102064
                DO  - 10.18632/aging.102064
                SP  - 4478
                EP  - 4509
                PY  - 
                AB  - Current clinical classification of hepatocellular carcinoma (HCC) is unable to predict prognosis efficiently. Our aim is to classify HCC into clinically/biologically relevant subtypes according to stromal factors. We detected seven types of stromal features in tumors from 161 HCC patients by immunohistochemical staining and Hematoxylin-eosin staining. Five stromal features were selected out of seven types of stromal features to construct stromal type based on LASSO COX regression model. Then, integrating multiple clinicopathologic characteristics and stromal type, we built two nomograms for overall survival (OS) and disease-free survival (DFS). Further validation of the stromal type and nomograms were performed in the testing cohort (n = 160) and validation cohort (n = 120). Using the LASSO model, we classified HCC patients into stromal type A subgroup (CD34lowTIL-stromal-ratiohighStromal-tumor-ratiolow&#x3B1;-SMAweakStromamature) and stromal type B subgroup (CD34highTIL-stromal-ratiolowStromal-tumor-ratiohigh&#x3B1;-SMAstrongStromaimmature). The stromal type was an independent prognostic factor for OS and DFS in the training, testing and validation cohorts. Two nomograms (for OS and DFS) that integrated the stromal type and clinicopathologic risk factors also showed good predictive accuracy and discriminatory power. In addition, immune cell recruitment in the tumor microenvironment (TME) was conditioned by the tumor stromal type. In conclusion, the newly developed tumor stromal type was an effective predictor of OS and DFS. Furthermore, the stromal type is associated with the immune phenotype in the TME.
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Serum retinol-binding protein 4 is associated with the presence and severity of coronary artery disease in patients with subclinical hypothyroidism

Hui-Xian Sun, Hui-Hong Ji, Xiao-Lin Chen, Li Wang, Yue Wang, Xi-Yu Shen, Xiang Lu, Wei Gao, Lian-Sheng Wang,

https://doi.org/10.18632/aging.102065 pp 4510—4520

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Sun H, Ji H, Chen X, Wang L, Wang Y, Shen X, Lu X, Gao W, Wang L, . Serum retinol-binding protein 4 is associated with the presence and severity of coronary artery disease in patients with subclinical hypothyroidism. . 11:4510-4520. https://doi.org/10.18632/aging.102065

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                TY  - JOUR
                AU  - Sun, Hui-Xian 
                AU  - Ji, Hui-Hong 
                AU  - Chen, Xiao-Lin 
                AU  - Wang, Li 
                AU  - Wang, Yue 
                AU  - Shen, Xi-Yu 
                AU  - Lu, Xiang 
                AU  - Gao, Wei 
                AU  - Wang, Lian-Sheng 
                TI  - Serum retinol-binding protein 4 is associated with the presence and severity of coronary artery disease in patients with subclinical hypothyroidism
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102065
                DO  - 10.18632/aging.102065
                SP  - 4510
                EP  - 4520
                PY  - 
                AB  - Subclinical hypothyroidism (SCH) plays a crucial role in the development and progression of coronary heart disease (CAD). Retinol-binding protein 4 (RBP4) is an adipokine correlated with cardiovascular diseases. Recent studies found that RBP4 levels are increased in patients with SCH. However, the relationship of RBP4 with CAD in SCH patients remains unclear. A total of 199 SCH patients (148 with CAD and 51 without CAD) and 102 healthy controls were enrolled in this study. Serum RBP4 was increased in SCH patients than controls. Moreover, serum RBP4 was higher in SCH patients with CAD. Although there was no significant difference of metabolic parameters between SCH patients with and without CAD, serum RBP4 was positively correlated with body mass index, total cholesterol, and low-density lipoprotein cholesterol, as well as thyroid stimulating hormone. Multivariable logistic regression analyses revealed elevated RBP4 was correlated with increased risk for CAD in SCH patients. Serum RBP4 levels were also increased as the number of stenosed vessels increased. Furthermore, increased RBP4 was positively correlated with the severity of CAD quantified by the Gensini score. Our findings demonstrate that serum RBP4 is associated with the presence and severity of CAD in patients with SCH.
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Genome-wide association study identifies CD1A associated with rate of increase in plasma neurofilament light in non-demented elders

Zuo-Teng Wang, Shi-Dong Chen, Wei Xu, Ke-Liang Chen, Hui-Fu Wang, Chen-Chen Tan, Mei Cui, Qiang Dong, Lan Tan, Jin-Tai Yu, Alzheimer’s Disease Neuroimaging Initiative,

https://doi.org/10.18632/aging.102066 pp 4521—4535

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Wang Z, Chen S, Xu W, Chen K, Wang H, Tan C, Cui M, Dong Q, Tan L, Yu J, , . Genome-wide association study identifies CD1A associated with rate of increase in plasma neurofilament light in non-demented elders. . 11:4521-4535. https://doi.org/10.18632/aging.102066

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                TY  - JOUR
                AU  - Wang, Zuo-Teng 
                AU  - Chen, Shi-Dong 
                AU  - Xu, Wei 
                AU  - Chen, Ke-Liang 
                AU  - Wang, Hui-Fu 
                AU  - Tan, Chen-Chen 
                AU  - Cui, Mei 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - Yu, Jin-Tai 
                AU  - ,  
                TI  - Genome-wide association study identifies CD1A associated with rate of increase in plasma neurofilament light in non-demented elders
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102066
                DO  - 10.18632/aging.102066
                SP  - 4521
                EP  - 4535
                PY  - 
                AB  - As a marker of neuroaxonal injury, neurofilament light (NFL) in blood is robustly elevated in many neurodegenerative conditions. We aimed to discover single nucleotide polymorphisms (SNPs) associated with longitudinal changes in plasma NFL levels that affect the risk of developing neurodegenerative disease and clinical disease progression. 545 eligible non-Hispanic white participants from the Alzheimer&#x2019;s Disease Neuroimaging Initiative (ADNI) with longitudinal plasma NFL data were included. Three SNPs (rs16840041, p=4.50&#xD7;10-8; rs2269714, p=4.50&#xD7;10-8; rs2269715, p=4.83&#xD7;10-8) in CD1A were in high linkage disequilibrium (LD) and significantly associated with the increase in plasma NFL levels. We demonstrate a promoting effect of rs16840041-A on clinical disease progression (p = 0.006). Moreover, the minor allele (A) of rs16840041 was significantly associated with accelerated decline in [18F] Fluorodeoxyglucose (FDG) (estimate -1.6% per year [95% CI -0.6 to -2.6], p=0.0024). CD1A is a gene involved in longitudinal changes in plasma NFL levels and AD-related phenotypes among non-demented elders. Given the potential effects of these variants, CD1A should be further investigated as a gene of interest in neurodegenerative diseases and as a potential target for monitoring disease trajectories and treating disease.
                ER  -

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Spontaneous γH2AX foci in human dermal fibroblasts in relation to proliferation activity and aging

Vadim Zorin, Anna Grekhova, Margarita Pustovalova, Alla Zorina, Nadezhda Smetanina, Natalia Vorobyeva, Pavel Kopnin, Ilmira Gilmutdinova, Alexey Moskalev, Andreyan N. Osipov, Sergey Leonov,

https://doi.org/10.18632/aging.102067 pp 4536—4546

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Zorin V, Grekhova A, Pustovalova M, Zorina A, Smetanina N, Vorobyeva N, Kopnin P, Gilmutdinova I, Moskalev A, Osipov AN, Leonov S, . Spontaneous γH2AX foci in human dermal fibroblasts in relation to proliferation activity and aging. . 11:4536-4546. https://doi.org/10.18632/aging.102067

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                TY  - JOUR
                AU  - Zorin, Vadim 
                AU  - Grekhova, Anna 
                AU  - Pustovalova, Margarita 
                AU  - Zorina, Alla 
                AU  - Smetanina, Nadezhda 
                AU  - Vorobyeva, Natalia 
                AU  - Kopnin, Pavel 
                AU  - Gilmutdinova, Ilmira 
                AU  - Moskalev, Alexey 
                AU  - Osipov, Andreyan N. 
                AU  - Leonov, Sergey 
                TI  - Spontaneous γH2AX foci in human dermal fibroblasts in relation to proliferation activity and aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102067
                DO  - 10.18632/aging.102067
                SP  - 4536
                EP  - 4546
                PY  - 
                AB  - We assessed the effects of donor age on clonogenicity, proliferative potential, and spontaneous &#x3B3;H2AX foci in the proliferating (Ki67 +) and senescent (SA &#x3B2;-gal +) cultures of skin fibroblasts isolated from 34 donors of different age (23-82 years). Here, we demonstrated that neither the colony forming effectiveness of proliferating (Ki67+) fraction of the fibroblasts nor the average number of &#x3B3;H2AX foci of the same fraction does not depend on the age of the donor. The correlation between the number of &#x3B3;H2AX foci and the donor&#x2019;s age was reliable in quiescent (Ki67-) cells. The average number of &#x3B3;H2AX foci in quiescent fibroblasts of donors older than 68 years was about two times higher than in the same cells of up to 30 years old donors. The number of &#x3B3;H2AX foci demonstrated a statistically significant positive correlation with the fraction of proliferating cells in fibroblast cultures. On average, proliferating cells have twice as many the &#x3B3;H2AX foci in comparison with the quiescent cells. Within a population of proliferating (Ki67+) cells, the degree of senescence correlated with a relative declining of constitutive &#x3B3;H2AX foci number, whereas in the population of quiescent (Ki67-) cells, it was proportional to augmenting the number of the &#x3B3;H2AX foci. Our data on a statistically significant (p=0.001) correlation between the age of the donor and the number of constitutive &#x3B3;H2AX foci in quiescent cells, could point out the ongoing DNA-damage response due in the maintenance of the senescent state of cells.
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Lower hand grip strength in older adults with non-alcoholic fatty liver disease: a nationwide population-based study

Beom-Jun Kim, Seong Hee Ahn, Seung Hun Lee, Seongbin Hong, Mark W. Hamrick, Carlos M. Isales, Jung-Min Koh,

https://doi.org/10.18632/aging.102068 pp 4547—4560

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Kim B, Ahn SH, Lee SH, Hong S, Hamrick MW, Isales CM, Koh J, . Lower hand grip strength in older adults with non-alcoholic fatty liver disease: a nationwide population-based study. . 11:4547-4560. https://doi.org/10.18632/aging.102068

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                TY  - JOUR
                AU  - Kim, Beom-Jun 
                AU  - Ahn, Seong Hee 
                AU  - Lee, Seung Hun 
                AU  - Hong, Seongbin 
                AU  - Hamrick, Mark W. 
                AU  - Isales, Carlos M. 
                AU  - Koh, Jung-Min 
                TI  - Lower hand grip strength in older adults with non-alcoholic fatty liver disease: a nationwide population-based study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102068
                DO  - 10.18632/aging.102068
                SP  - 4547
                EP  - 4560
                PY  - 
                AB  - Although both liver and muscle are metabolically active endocrine organs, and non-alcoholic fatty liver disease (NAFLD) and sarcopenia may share common pathogenic determinants, there have been few clinical studies of the relationship between NAFLD and muscle strength, especially in the elderly. We conducted a nationally representative population-based, cross-sectional study using data from the Korea National Health and Nutrition Examination Survey, which involved 1,897 men aged &#x2265;50 years and 2,206 postmenopausal women. NAFLD was defined using the hepatic steatosis index (HSI) and low muscle strength was defined using the Korea-specific cut-off point of hand grip strength (HGS). Men and women with NAFLD had 7.3% and 7.9% lower HGS than controls, respectively. The odds ratios for low muscle strength in the presence of NAFLD were 2.51 in men and 2.34 in women. HSI inversely correlated with HGS in both men and women. Consistently, compared with men and women in the lowest HSI quartile, those in the highest quartile had 7.6% and 12.4% lower HGS, respectively, and were 5.63- and 3.58-times more likely to have low muscle strength, respectively. These results provide the first clinical evidence that NAFLD can be associated with muscular impairment in older adults, as demonstrated by lower muscle strength.
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Enhanced beta-1 adrenergic receptor responsiveness in coronary arterioles following intravenous stromal vascular fraction therapy in aged rats

Gabrielle Rowe, Natia Q. Kelm, Jason E. Beare, Evan Tracy, Fangping Yuan, Amanda J. LeBlanc,

https://doi.org/10.18632/aging.102069 pp 4561—4578

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Rowe G, Kelm NQ, Beare JE, Tracy E, Yuan F, LeBlanc AJ, . Enhanced beta-1 adrenergic receptor responsiveness in coronary arterioles following intravenous stromal vascular fraction therapy in aged rats. . 11:4561-4578. https://doi.org/10.18632/aging.102069

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                TY  - JOUR
                AU  - Rowe, Gabrielle 
                AU  - Kelm, Natia Q. 
                AU  - Beare, Jason E. 
                AU  - Tracy, Evan 
                AU  - Yuan, Fangping 
                AU  - LeBlanc, Amanda J. 
                TI  - Enhanced beta-1 adrenergic receptor responsiveness in coronary arterioles following intravenous stromal vascular fraction therapy in aged rats
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102069
                DO  - 10.18632/aging.102069
                SP  - 4561
                EP  - 4578
                PY  - 
                AB  - Our past study showed that a single tail vein injection of adipose-derived stromal vascular fraction (SVF) into old rats was associated with improved dobutamine-mediated coronary flow reserve. We hypothesize that i.v. injection of SVF improves coronary microvascular function in aged rats via alterations in beta adrenergic microvascular signaling. Female Fischer-344 rats aged young (3 months, n=32) and old (24 months, n=30) were utilized, along with two cell therapies intravenously injected in old rats four weeks prior to sacrifice: 1x107 green fluorescent protein (GFP+) SVF cells (O+SVF, n=21), and 5x106 GFP+ bone-marrow mesenchymal stromal cells (O+BM, n=6), both harvested from young donors. Cardiac ultrasound and pressure-volume measurements were obtained, and coronary arterioles were isolated from each group for microvessel reactivity studies and immunofluorescence staining. Coronary flow reserve decreased with advancing age, but this effect was rescued by the SVF treatment in the O+SVF group. Echocardiography showed an age-related diastolic dysfunction that was improved with SVF to a greater extent than with BM treatment. Coronary arterioles isolated from SVF-treated rats showed amelioration of the age-related decrease in vasodilation to a non-selective &#x3B2;-AR agonist. I.v. injected SVF cells improved &#x3B2;-adrenergic receptor-dependent coronary flow and microvascular function in a model of advanced age.
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Ketones improves Apolipoprotein E4-related memory deficiency via sirtuin 3

Junxiang Yin, Megan Nielsen, Shiping Li, Jiong Shi,

https://doi.org/10.18632/aging.102070 pp 4579—4586

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Yin J, Nielsen M, Li S, Shi J, . Ketones improves Apolipoprotein E4-related memory deficiency via sirtuin 3. . 11:4579-4586. https://doi.org/10.18632/aging.102070

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                TY  - JOUR
                AU  - Yin, Junxiang 
                AU  - Nielsen, Megan 
                AU  - Li, Shiping 
                AU  - Shi, Jiong 
                TI  - Ketones improves Apolipoprotein E4-related memory deficiency via sirtuin 3
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102070
                DO  - 10.18632/aging.102070
                SP  - 4579
                EP  - 4586
                PY  - 
                AB  - Background: Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimer&#x2019;s disease (AD). ApoE4 carriers have cerebral hypometabolism which is thought as a harbinger of AD. Our previous studies indicated ketones improved mitochondria energy metabolism via sirtuin 3 (Sirt3). However, it is unclear whether ketones upregulate Sirt3 and improve ApoE4-related learning and memory deficits.Results: Ketones improved learning and memory abilities of ApoE4 mice but not ApoE3 mice. Sirt3, synaptic proteins, the NAD+/ NADH ratio, and ATP production were significantly increased in the hippocampus and the cortex from ketone treatment.Methods: Human ApoE3 and ApoE4 transgenic mice (9-month-old) were treated with either ketones or normal saline by daily subcutaneous injections for 3 months (ketones, beta-hydroxybutyrate (BHB): 600 mg/kg/day; acetoacetate (ACA): 150 mg/kg/day). Learning and memory ability of these mice were assessed. Sirt3 protein, synaptic proteins (PSD95, Synaptophysin), the NAD+/ NADH ratio, and ATP levels were measured in the hippocampus and the cortex.Conclusion: Our current studies suggest that ketones improve learning and memory abilities of ApoE4 transgenic mice. Sirt3 may mediate the neuroprotection of ketones by increasing neuronal energy metabolism in ApoE4 transgenic mice. This provides the foundation for Sirt3&#x2019;s potential role in the prevention and treatment of AD.
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LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling

Wenmei Su, Chunfang Guo, Lihui Wang, Zhuwen Wang, Xia Yang, Feiyu Niu, Daniel Tzou, Xiao Yang, Xiaobi Huang, Jiancong Wu, Xiaorao Chen, Lei Zou, Zhixiong Yang, Guoan Chen,

https://doi.org/10.18632/aging.102071 pp 4587—4596

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Su W, Guo C, Wang L, Wang Z, Yang X, Niu F, Tzou D, Yang X, Huang X, Wu J, Chen X, Zou L, Yang Z, et al, . LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling. . 11:4587-4596. https://doi.org/10.18632/aging.102071

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Provider: 
 TY - JOUR
 AU - Su, Wenmei 
 AU - Guo, Chunfang 
 AU - Wang, Lihui 
 AU - Wang, Zhuwen 
 AU - Yang, Xia 
 AU - Niu, Feiyu 
 AU - Tzou, Daniel 
 AU - Yang, Xiao 
 AU - Huang, Xiaobi 
 AU - Wu, Jiancong 
 AU - Chen, Xiaorao 
 AU - Zou, Lei 
 AU - Yang, Zhixiong 
 AU - Chen, Guoan 
 TI - LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling
 JO - 
 JA - 
 VL - 11
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102071
 DO - 10.18632/aging.102071
 SP - 4587
 EP - 4596
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Su, Wenmei 
 AU - Guo, Chunfang 
 AU - Wang, Lihui 
 AU - Wang, Zhuwen 
 AU - Yang, Xia 
 AU - Niu, Feiyu 
 AU - Tzou, Daniel 
 AU - Yang, Xiao 
 AU - Huang, Xiaobi 
 AU - Wu, Jiancong 
 AU - Chen, Xiaorao 
 AU - Zou, Lei 
 AU - Yang, Zhixiong 
 AU - Chen, Guoan 
 TI - LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling
 JO - 
 JA - 
 VL - 11
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102071
 DO - 10.18632/aging.102071
 SP - 4587
 EP - 4596
 PY - 
 AB - Long non-coding RNAs (lncRNAs) have involved in human malignancies and played an important role in gene regulations. The dysregulation of lncRNA MIR22HG has been reported in several cancers. However, the role of MIR22HG in esophageal adenocarcinoma (EAC) is poorly understood. Loss of function approaches were used to investigate the biological role of MIR22HG in EAC cells. The effects of MIR22HG on cell proliferation were evaluated by WST-1 and colony formation assays. The effects of MIR22HG on cell migration and invasion were examined using transwell assays. QRT-PCR and Western blot were used to evaluate the mRNA and protein expression of related genes. In this study, abrogation of MIR22HG inhibited cell proliferation, colony formation, invasion and migration in EAC 3 cell lines (OE33, OE19 and FLO-1). Mechanistically, MIR22HG silencing decreased the expression of STAT3/c-Myc/p-FAK proteins and induced apoptosis in EAC cell lines. These results delineate a novel mechanism of MIR22HG in EAC, and may provide potential targets by developing lncRNA-based therapies for EAC.
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Role of microtubule-associated protein 6 glycosylated with Gal-(β-1,3)-GalNAc in Parkinson's disease

Li Ma, Jiaxin Song, Xueying Sun, Wenyong Ding, Kaiyang Fan, Minghua Qi, Yuefei Xu, Wenli Zhang,

https://doi.org/10.18632/aging.102072 pp 4597—4610

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Ma L, Song J, Sun X, Ding W, Fan K, Qi M, Xu Y, Zhang W, . Role of microtubule-associated protein 6 glycosylated with Gal-(β-1,3)-GalNAc in Parkinson's disease. . 11:4597-4610. https://doi.org/10.18632/aging.102072

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                TY  - JOUR
                AU  - Ma, Li 
                AU  - Song, Jiaxin 
                AU  - Sun, Xueying 
                AU  - Ding, Wenyong 
                AU  - Fan, Kaiyang 
                AU  - Qi, Minghua 
                AU  - Xu, Yuefei 
                AU  - Zhang, Wenli 
                TI  - Role of microtubule-associated protein 6 glycosylated with Gal-(β-1,3)-GalNAc in Parkinson's disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102072
                DO  - 10.18632/aging.102072
                SP  - 4597
                EP  - 4610
                PY  - 
                AB  - Aberrant glycosylation of proteins has major implications for human diseases. To determine whether protein glycosylation contributes to the pathogenesis of Parkinson&#x2019;s disease (PD), a mouse model of PD was established by injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Induction of PD-like features was verified by assessing motor impairment and confirming reductions in biological markers, including dopamine, 5-hydroxytryptamine and tyrosine hydroxylase, as well as the aggregation of &#x3B1;-synuclein. Altered glycosylation was detected using biotinylated agaracus bisporus lectin, which specifically binds exposed Gal-(&#x3B2;-1,3)-GalNAc linked to glycoproteins. Subsequent lectin affinity chromatography coupled with mass spectrometry revealed enhanced glycosylation of microtubule-associated protein 6 (MAP6) in PD mice as compared to healthy controls. In situ dual co-immunofluorescence analysis and immunoblotting confirmed that MAP6 is glycosylated with Gal-(&#x3B2;-1,3)-GalNAc oligosaccharides, which in turn alters the distribution and structure of MAP6 complexes within neurons. This is the first study to described MAP6 as a glycoprotein containing Gal-(&#x3B2;-1,3)-GalNAc oligosaccharides and to show that hyperglycosylation of MAP6 is strongly associated with the pathogenesis of PD. These findings provide potentially valuable information for developing new therapeutic targets for the treatment of PD as well as reliably prognostic biomarkers.
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The role of commensal microbes in the lifespan of Drosophila melanogaster

Hye-Yeon Lee, Shin-Hae Lee, Ji-Hyeon Lee, Won-Jae Lee, Kyung-Jin Min,

https://doi.org/10.18632/aging.102073 pp 4611—4640

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Lee H, Lee S, Lee J, Lee W, Min K, . The role of commensal microbes in the lifespan of Drosophila melanogaster. . 11:4611-4640. https://doi.org/10.18632/aging.102073

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 TY - JOUR
 AU - Lee, Hye-Yeon 
 AU - Lee, Shin-Hae 
 AU - Lee, Ji-Hyeon 
 AU - Lee, Won-Jae 
 AU - Min, Kyung-Jin 
 TI - The role of commensal microbes in the lifespan of Drosophila melanogaster
 JO - 
 JA - 
 VL - 11
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102073
 DO - 10.18632/aging.102073
 SP - 4611
 EP - 4640
 PY - 
 AB - Commensal microbes have mutualistic relationships with their host and mainly live in the host intestine. There are many studies on the relationships between commensal microbes and host physiology. However, there are inconsistent results on the effects of commensal microbes on host lifespan. To clarify this controversy, we generated axenic flies by using two controlled methods &#x2013; bleaching and antibiotic treatment &#x2013; and investigated the relationship between the commensal microbes and host lifespan in Drosophila melanogaster. The removal of microbes by using bleaching and antibiotic treatments without detrimental effects increased fly lifespan. Furthermore, a strain of flies colonized with a high load of microbiota showed a greater effect on lifespan extension when the microbes were eliminated, suggesting that commensal bacteria abundance may be a critical determinant of host lifespan. Consistent with those observations, microbial flora of aged fly gut significantly decreased axenic fly lifespan via an increase in bacterial load rather than through a change of bacterial composition. Our elaborately controlled experiments showed that the elimination of commensal microbes without detrimental side effects increased fly lifespan, and that bacterial load was a significant determinant of lifespan. Furthermore, our results indicate the presence of a deterministic connection between commensal microbes and host lifespan.
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Age-associated changes of the intrinsic nervous system in relation with interstitial cells in the pre-weaning goat rumen

Yu Liang, Imran Tarique, Waseem Ail Vistro, Yifei Liu, Ziyu Wang, Abdul haseeb, Noor Samad Gandahi, Adeela Iqbal, Siyi Wang, Tianci An, Huan Yang, Qiusheng Chen, Ping Yang,

https://doi.org/10.18632/aging.102076 pp 4641—4653

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Liang Y, Tarique I, Vistro WA, Liu Y, Wang Z, haseeb A, Gandahi NS, Iqbal A, Wang S, An T, Yang H, Chen Q, Yang P, . Age-associated changes of the intrinsic nervous system in relation with interstitial cells in the pre-weaning goat rumen. . 11:4641-4653. https://doi.org/10.18632/aging.102076

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                TY  - JOUR
                AU  - Liang, Yu 
                AU  - Tarique, Imran 
                AU  - Vistro, Waseem Ail 
                AU  - Liu, Yifei 
                AU  - Wang, Ziyu 
                AU  - haseeb, Abdul 
                AU  - Gandahi, Noor Samad 
                AU  - Iqbal, Adeela 
                AU  - Wang, Siyi 
                AU  - An, Tianci 
                AU  - Yang, Huan 
                AU  - Chen, Qiusheng 
                AU  - Yang, Ping 
                TI  - Age-associated changes of the intrinsic nervous system in relation with interstitial cells in the pre-weaning goat rumen
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102076
                DO  - 10.18632/aging.102076
                SP  - 4641
                EP  - 4653
                PY  - 
                AB  - In this study, we investigated the neural changes and their relationships with interstitial cells (ICs) in the rumen of pre-weaning goats by transmission electron microscopy, western blot and immunofluorescence (antibody: general neuronal marker-Protein Gene Product (PGP9.5)/ IC marker-vimentin). The immunofluorescence results showed that PGP9.5-positive reaction was widely distributed in neuronal soma (NS) and nerve fibre (NF). The NSs were observed in the ganglia of the myenteric plexus (MP) but not in the submucosal plexus. The mean optical density (MOD) of the whole of PGP9.5-positive nerves and the protein expression level of PGP.5 in the rumen wall both decreased significantly with age. However an obvious increase MOD of PGP.5-positive NFs within the rumen epithelium were observed. In the MP, the nerves and ICs were interwoven to form two complex networks that gradually tightened with age. Furthermore, NSs and nerve trunks were surrounded by a ring-boundary layer consisting of several ICs that became physically closer with aging. Moreover, ICs were located nearby NFs within the ML, forming connections between ICs, smooth muscle cells and axons. This study describes the pattern of neural distribution and its association with ICs in the developing rumen which shed light on the postpartum development of ruminants.
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Ambient particulate matter attenuates Sirtuin1 and augments SREBP1-PIR axis to induce human pulmonary fibroblast inflammation: molecular mechanism of microenvironment associated with COPD

Chia-Ping Tien, Chia-Hung Chen, Wen-Yuan Lin, Chiu-Shong Liu, Ko-Jiunn Liu, Michael Hsiao, Yu-Chan Chang, Shih-Chieh Hung,

https://doi.org/10.18632/aging.102077 pp 4654—4671

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Tien C, Chen C, Lin W, Liu C, Liu K, Hsiao M, Chang Y, Hung S, . Ambient particulate matter attenuates Sirtuin1 and augments SREBP1-PIR axis to induce human pulmonary fibroblast inflammation: molecular mechanism of microenvironment associated with COPD. . 11:4654-4671. https://doi.org/10.18632/aging.102077

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                TY  - JOUR
                AU  - Tien, Chia-Ping 
                AU  - Chen, Chia-Hung 
                AU  - Lin, Wen-Yuan 
                AU  - Liu, Chiu-Shong 
                AU  - Liu, Ko-Jiunn 
                AU  - Hsiao, Michael 
                AU  - Chang, Yu-Chan 
                AU  - Hung, Shih-Chieh 
                TI  - Ambient particulate matter attenuates Sirtuin1 and augments SREBP1-PIR axis to induce human pulmonary fibroblast inflammation: molecular mechanism of microenvironment associated with COPD
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102077
                DO  - 10.18632/aging.102077
                SP  - 4654
                EP  - 4671
                PY  - 
                AB  - Evidences have shown a strong link between particulate matter (PM) and increased risk in human mortality and morbidity, including asthma, chronic obstructive pulmonary disease (COPD), respiratory infection, and lung cancer. However, the underlying toxicologic mechanisms remain largely unknown. Utilizing PM-treated human pulmonary fibroblasts (HPF) models, we analyzed gene expression microarray data and Ingenuity Pathway Analysis (IPA) to identify that the transcription factor sterol regulatory element-binding protein 1 (SREBP1) was the main downstream regulator of Sirtuin1 (SIRT1). Quantitative PCR and western blot results showed that SIRT1 inhibited SREBP1 and further downregulated Pirin (PIR) and Nod-like receptor protein 3 (NLRP3) inflammasome after PM exposure. Inhibitors of SIRT1, SREBP1, and PIR could reverse PM-induced inflammation. An in silico analysis revealed that PIR correlated with smoke exposure and early COPD. Immunohistochemical analysis of tissue microarrays from PM-fed mouse models was used to determine the association of PIR with PM. These data demonstrate that the SIRT1-SREBP1-PIR/ NLRP3 inflammasome axis may be associated with PM-induced adverse health issues. SIRT1 functions as a protector from PM exposure, whereas PIR acts as a predictor of PM-induced pulmonary disease. The SIRT1-SREBP1-PIR/ NLRP3 inflammasome axis may present several potential therapeutic targets for PM-related adverse health events.
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Genome-wide association and evolutionary analyses reveal the formation of swine facial wrinkles in Chinese Erhualian pigs

Tao Huang, Mingpeng Zhang, Guorong Yan, Xiaochang Huang, Hao Chen, Liyu Zhou, Wenjiang Deng, Zhen Zhang, Hengqing Qiu, Huashui Ai, Lusheng Huang,

https://doi.org/10.18632/aging.102078 pp 4672—4687

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Huang T, Zhang M, Yan G, Huang X, Chen H, Zhou L, Deng W, Zhang Z, Qiu H, Ai H, Huang L, . Genome-wide association and evolutionary analyses reveal the formation of swine facial wrinkles in Chinese Erhualian pigs. . 11:4672-4687. https://doi.org/10.18632/aging.102078

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                TY  - JOUR
                AU  - Huang, Tao 
                AU  - Zhang, Mingpeng 
                AU  - Yan, Guorong 
                AU  - Huang, Xiaochang 
                AU  - Chen, Hao 
                AU  - Zhou, Liyu 
                AU  - Deng, Wenjiang 
                AU  - Zhang, Zhen 
                AU  - Qiu, Hengqing 
                AU  - Ai, Huashui 
                AU  - Huang, Lusheng 
                TI  - Genome-wide association and evolutionary analyses reveal the formation of swine facial wrinkles in Chinese Erhualian pigs
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102078
                DO  - 10.18632/aging.102078
                SP  - 4672
                EP  - 4687
                PY  - 
                AB  - Wrinkles are uneven concave-convex folds, ridges or creases in skin. Facial wrinkles appear in head, typically increasing along with aging. However in several Chinese indigenous pigs, such as Erhualian pigs, rich facial wrinkles have been generated during the growth stages as one of their breed characteristics. To investigate the genetic basis underlying the development of swine facial wrinkles, we estimated the folding extent of facial wrinkles in a herd of Erhualian pigs (n=332), and then conducted genome-wide association studies and multi-trait meta-analysis for facial wrinkles using 60K porcine chips. We found that facial wrinkles had high heritability estimates of ~0.7 in Erhualian pigs. Notably, only one genome-wide significant QTL was detected at 34.8 Mb on porcine chromosome 7. The most significant SNP rs80983858 located at the 3255-bp downstream of candidate gene GRM4, and the G allele was of benefit to increase facial wrinkles. Evolutionary and selection analyses suggested that the haplotypes containing G allele were under artificial selection, which was consistent with local animal sacrificial custom praying for longevity. Our findings made important clues for further deciphering the molecular mechanism of swine facial wrinkles formation, and shed light on the research of skin wrinkle development in human or other mammals.
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Assessment of ERBB2 and TOP2α gene status and expression profile in feline mammary tumors: findings and guidelines

Daniela Ferreira, Maria Soares, Jorge Correia, Filomena Adega, Fernando Ferreira, Raquel Chaves,

https://doi.org/10.18632/aging.102079 pp 4688—4705

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Ferreira D, Soares M, Correia J, Adega F, Ferreira F, Chaves R, . Assessment of ERBB2 and TOP2α gene status and expression profile in feline mammary tumors: findings and guidelines. . 11:4688-4705. https://doi.org/10.18632/aging.102079

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Provider: 
 TY - JOUR
 AU - Ferreira, Daniela 
 AU - Soares, Maria 
 AU - Correia, Jorge 
 AU - Adega, Filomena 
 AU - Ferreira, Fernando 
 AU - Chaves, Raquel 
 TI - Assessment of ERBB2 and TOP2α gene status and expression profile in feline mammary tumors: findings and guidelines
 JO - 
 JA - 
 VL - 11
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102079
 DO - 10.18632/aging.102079
 SP - 4688
 EP - 4705
 PY - 
 AB - In humans, the ERBB2 gene amplification and overexpression are biomarkers for invasive breast cancer and a therapeutic target. Also, TOP2&#x3B1; gene aberrations predict the response to anthracycline-based adjuvant chemotherapy. Although feline mammary tumors (FMTs) are good models in comparative oncology, scarce data is available regarding the ERBB2 and TOP2&#x3B1; status. In this study, and for the first time, the ERBB2 DNA status and RNA levels of intracellular (ICD) and extracellular (ECD) coding regions were compared with TOP2&#x3B1; gene status and expression profile, in samples of FMTs and disease-free tissues from the same animal. Results showed that ERBB2 and TOP2&#x3B1; gene status are highly correlated (r=0.87, p&lt;0.0001, n=25), with few tumor samples presenting amplification. Also, the majority of the FMTs showed ERBB2 overexpression coupled with TOP2&#x3B1; overexpression (r=0.87, p&lt;0.0001, n=27), being the ERBB2-ICD and ECD transcripts highly correlated (r=0.97, p&lt;0.0001, n=27). Significant associations were found between TOP2&#x3B1; gene status or ERBB2 and TOP2&#x3B1; RNA levels with several clinicopathological parameters. This work highlights the need of experimental designs for a precise evaluation of ERBB2 and TOP2&#x3B1; gene status and its expression in FMTs, to improve their clinical management and to further validate them as a suitable model for comparative oncology studies.
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Tea polyphenol protects against cisplatin-induced meiotic defects in porcine oocytes

Changyin Zhou, Xue Zhang, Xiayan ShiYang, Huili Wang, Bo Xiong,

https://doi.org/10.18632/aging.102084 pp 4706—4719

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Zhou C, Zhang X, ShiYang X, Wang H, Xiong B, . Tea polyphenol protects against cisplatin-induced meiotic defects in porcine oocytes. . 11:4706-4719. https://doi.org/10.18632/aging.102084

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                TY  - JOUR
                AU  - Zhou, Changyin 
                AU  - Zhang, Xue 
                AU  - ShiYang, Xiayan 
                AU  - Wang, Huili 
                AU  - Xiong, Bo 
                TI  - Tea polyphenol protects against cisplatin-induced meiotic defects in porcine oocytes
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102084
                DO  - 10.18632/aging.102084
                SP  - 4706
                EP  - 4719
                PY  - 
                AB  - DDP (cisplatin), a DNA cross-linking agent, is one of the most common chemotherapeutic drugs that have been widely used in the treatment of sarcomas and germ cell tumors. DDP treatment exhibits severe side effects including renal toxicity, ototoxicity and embryo-toxicity. Women of reproductive age treated with DDP may lead to loss of primordial follicles, resulting in the depletion of the ovarian reserve and consequent premature ovarian failure. However, the influence of DDP on the oocyte quality and the strategy to prevent it has not yet fully clarified. Here, we report that DDP exposure resulted in the oocyte meiotic failure via disrupting the meiotic organelle dynamics and arrangement, exhibiting a prominently impaired cytoskeleton assembly, including spindle formation and actin polymerization. In addition, exposure to DDP led to the abnormal distribution of mitochondrion and cortical granules, two indicators of cytoplasmic maturation of oocytes. Conversely, TP (tea polyphenols) supplementation partially restored all of the meiotic defects resulted from DDP exposure through suppressing the increase of ROS level and the occurrence of DNA damage as well as apoptosis.
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Alternative splicing events are prognostic in hepatocellular carcinoma

Qi-Feng Chen, Wang Li, Peihong Wu, Lujun Shen, Zi-Lin Huang,

https://doi.org/10.18632/aging.102085 pp 4720—4735

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Chen Q, Li W, Wu P, Shen L, Huang Z, . Alternative splicing events are prognostic in hepatocellular carcinoma. . 11:4720-4735. https://doi.org/10.18632/aging.102085

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                TY  - JOUR
                AU  - Chen, Qi-Feng 
                AU  - Li, Wang 
                AU  - Wu, Peihong 
                AU  - Shen, Lujun 
                AU  - Huang, Zi-Lin 
                TI  - Alternative splicing events are prognostic in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102085
                DO  - 10.18632/aging.102085
                SP  - 4720
                EP  - 4735
                PY  - 
                AB  - Alternative splicing events (ASEs) play a role in cancer development and progression. We investigated whether ASEs are prognostic for overall survival (OS) in hepatocellular carcinoma (HCC). RNA sequencing data was obtained for 343 patients included in The Cancer Genome Atlas. Matched splicing event data for these patients was then obtained from the TCGASpliceSeq database, which includes data for seven types of ASEs. Univariate and multivariate Cox regression analysis demonstrated that 3,814 OS-associated splicing events (OS-SEs) were correlated with OS. Prognostic indices were developed based on the most significant OS-SEs. The prognostic index based on all seven types of ASEs (PI-ALL) demonstrated superior efficacy in predicting OS of HCC patients at 2,000 days compared to those based on single ASE types. Patients were stratified into two risk groups (high and low) based on the median prognostic index. Kaplan-Meier survival analysis demonstrated that PI-ALL had the greatest capacity to distinguish between patients with favorable vs. poor outcomes. Finally, univariate Cox regression analysis demonstrated that the expression of 23 splicing factors was correlated with OS-SEs in the HCC cohort. Our data indicate that a prognostic index based on ASEs is prognostic for OS in HCC.
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Identification of hub genes in prostate cancer using robust rank aggregation and weighted gene co-expression network analysis

Zhen-yu Song, Fan Chao, Zhiyuan Zhuo, Zhe Ma, Wenzhi Li, Gang Chen,

https://doi.org/10.18632/aging.102087 pp 4736—4756

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Song Z, Chao F, Zhuo Z, Ma Z, Li W, Chen G, . Identification of hub genes in prostate cancer using robust rank aggregation and weighted gene co-expression network analysis. . 11:4736-4756. https://doi.org/10.18632/aging.102087

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                TY  - JOUR
                AU  - Song, Zhen-yu 
                AU  - Chao, Fan 
                AU  - Zhuo, Zhiyuan 
                AU  - Ma, Zhe 
                AU  - Li, Wenzhi 
                AU  - Chen, Gang 
                TI  - Identification of hub genes in prostate cancer using robust rank aggregation and weighted gene co-expression network analysis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102087
                DO  - 10.18632/aging.102087
                SP  - 4736
                EP  - 4756
                PY  - 
                AB  - The pathogenic mechanisms of prostate cancer (PCa) remain to be defined. In this study, we utilized the Robust Rank Aggregation (RRA) method to integrate 10 eligible PCa microarray datasets from the GEO and identified a set of significant differentially expressed genes (DEGs) between tumor samples and normal, matched specimens. To explore potential associations between gene sets and PCa clinical features and to identify hub genes, we utilized WGCNA to construct gene co-expression networks incorporating the DEGs screened with the use of RRA. From the key module, we selected LMNB1, TK1, ZWINT, and RACGAP1 for validation. We found that these genes were up-regulated in PCa samples, and higher expression levels were associated with higher Gleason scores and tumor grades. Moreover, ROC and K-M plots indicated these genes had good diagnostic and prognostic value for PCa. On the other hand, methylation analyses suggested that the abnormal up-regulation of these four genes likely resulted from hypomethylation, while GSEA and GSVA for single hub gene revealed they all had a close association with proliferation of PCa cells. These findings provide new insight into PCa pathogenesis, and identify LMNB1, TK1, RACGAP1 and ZWINT as candidate biomarkers for diagnosis and prognosis of PCa.
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Circular RNAs in leukemia

Zijuan Wu, Handong Sun, Jianyong Li, Hui Jin,

https://doi.org/10.18632/aging.102091 pp 4757—4771

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Wu Z, Sun H, Li J, Jin H, . Circular RNAs in leukemia. . 11:4757-4771. https://doi.org/10.18632/aging.102091

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                TY  - JOUR
                AU  - Wu, Zijuan 
                AU  - Sun, Handong 
                AU  - Li, Jianyong 
                AU  - Jin, Hui 
                TI  - Circular RNAs in leukemia
                JO  - 
                JA  - 
                VL  - 11
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102091
                DO  - 10.18632/aging.102091
                SP  - 4757
                EP  - 4771
                PY  - 
                AB  - In pace with the development of gene sequencing technology and transcriptome research, it has been found that 70 to 90% of the human genome is transcribed into RNAs, while only 2% of RNAs encode proteins. This implies that non-coding RNAs (ncRNAs) may exert vital biological functions and a full analysis of non-coding transcriptomes is needed. Over the past decade, the advance in high-throughput sequencing and transcriptome profiling has enabled the identification of circular RNAs (circRNAs) involved in many biological processes and the occurrence and development of diseases. Accumulating evidence has revealed that circRNAs may serve as new biomarkers for diagnosis as well as provide promising therapeutic approaches and novel drug screening strategies for leukemia. A comprehensive understanding of circRNAs in leukemia is a prerequisite for the development of clinical translational research. In this review, we will discuss the general information of circRNAs and focus on the current advances in understanding the association between dysregulated circRNAs and leukemia.
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Volume 11, Issue 13

About the Cover

Editorials

Miroslav Balaz, Christian Wolfrum,

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Behnam N. Tehrani, Carolyn M. Rosner, Wayne B. Batchelor,

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Keyvan Yousefi, Julian C. Dunkley, Lina A. Shehadeh,

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Jiri Neuzil, Michael V. Berridge,

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Research Papers

Dong Cheng, Yi Tang, Haiyu Li, Yunpeng Li, Haiqiang Sang,

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Shuo Sun, Bincui Cai, Yao Li, Wenqi Su, Xuzheng Zhao, Boteng Gong, Zhiqing Li, Xiaomin Zhang, Yalin Wu, Chao Chen, Stephen H. Tsang, Jin Yang, Xiaorong Li,

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Juan Ji, Ting Fu, Chen Dong, Wenyan Zhu, Junling Yang, Xiaoli Kong, Zhongyuan Zhang, Yanfeng Bao, Rui Zhao, Xinyu Ge, Xiaoqi Sha, Zhimin Lu, Jing Li, Zhifeng Gu,

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Zhenbin Cai, Xiaonan Zhu, Guowei Zhang, Fengming Wu, Hongsheng Lin, Minghui Tan,

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Raj K. Kurupati, Larissa H. Haut, Kenneth E. Schmader, Hildegund CJ. Ertl,

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Qi Jia, Hongbo Nie, Peng Yu, Baiyun Xie, Chenji Wang, Fu Yang, Gang Wei, Ting Ni,

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Hao Zi, Xue-Jun Wang, Ming-Juan Zhao, Qiao Huang, Xing-Huan Wang, Xian-Tao Zeng,

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Feng Gao, Xie-lin Huang, Meng-Xing Cai, Miao-tong Lin, Bin-feng Wang, Wei Wu, Zhi-Ming Huang,

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Zhi-Hui Li, Yi-Fei Wang, Dan-Dan He, Xue-Mei Zhang, Ying-Lian Zhou, Hui Yue, Shan Huang, Zheng Fu, Ling-Yu Zhang, Zhu-Qing Mao, Shuang Li, Chen-Yu Zhang, Xi Chen, Jin Fu,

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Wei Li, Jun Han, Kefei Yuan, Hong Wu,

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Hui-Xian Sun, Hui-Hong Ji, Xiao-Lin Chen, Li Wang, Yue Wang, Xi-Yu Shen, Xiang Lu, Wei Gao, Lian-Sheng Wang,

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Zuo-Teng Wang, Shi-Dong Chen, Wei Xu, Ke-Liang Chen, Hui-Fu Wang, Chen-Chen Tan, Mei Cui, Qiang Dong, Lan Tan, Jin-Tai Yu, Alzheimer’s Disease Neuroimaging Initiative,

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Vadim Zorin, Anna Grekhova, Margarita Pustovalova, Alla Zorina, Nadezhda Smetanina, Natalia Vorobyeva, Pavel Kopnin, Ilmira Gilmutdinova, Alexey Moskalev, Andreyan N. Osipov, Sergey Leonov,

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Beom-Jun Kim, Seong Hee Ahn, Seung Hun Lee, Seongbin Hong, Mark W. Hamrick, Carlos M. Isales, Jung-Min Koh,

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Gabrielle Rowe, Natia Q. Kelm, Jason E. Beare, Evan Tracy, Fangping Yuan, Amanda J. LeBlanc,