Volume 10, Issue 3

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                TY  - JOUR
                AU  - Chu, Yu-Lan 
                AU  - Xu, Ya-Ru 
                AU  - Yang, Wan-Xi 
                AU  - Sun, Yi 
                TI  - The role of FSH and TGF-β superfamily in follicle atresia
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101391
                DO  - 10.18632/aging.101391
                SP  - 305
                EP  - 321
                PY  - 
                AB  - Most of the mammalian follicles undergo a degenerative process called “follicle atresia”. Apoptosis of granulosa cells is the main characteristic of follicle atresia. Follicle stimulating hormone (FSH) and the transforming growth factor β (TGF-β) superfamily have important regulatory functions in this process. FSH activates protein kinase A and cooperating with insulin receptor substrates, it promotes the PI3K/Akt pathway which weakens apoptosis. Both Smad or non-Smad signaling of the transforming growth factor β superfamily seem to be related to follicle atresia, and the effect of several important family members on follicle atresia is concluded in this article. FSH and TGF-β are likely to mutually influence each other and what we have already known about the possible underlying molecular mechanism is also discussed below.
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Deficiency in DNA damage response of enterocytes accelerates intestinal stem cell aging in Drosophila

Joung-Sun Park, Ho-Jun Jeon, Jung-Hoon Pyo, Young-Shin Kim, Mi-Ae Yoo,

https://doi.org/10.18632/aging.101390 pp 322—338

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Park J, Jeon H, Pyo J, Kim Y, Yoo M, . Deficiency in DNA damage response of enterocytes accelerates intestinal stem cell aging in Drosophila. . 10:322-338. https://doi.org/10.18632/aging.101390

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                TY  - JOUR
                AU  - Park, Joung-Sun 
                AU  - Jeon, Ho-Jun 
                AU  - Pyo, Jung-Hoon 
                AU  - Kim, Young-Shin 
                AU  - Yoo, Mi-Ae 
                TI  - Deficiency in DNA damage response of enterocytes accelerates intestinal stem cell aging in <i>Drosophila</i>
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101390
                DO  - 10.18632/aging.101390
                SP  - 322
                EP  - 338
                PY  - 
                AB  - Stem cell dysfunction is closely linked to tissue and organismal aging and age-related diseases, and heavily influenced by the niche cells’ environment. The DNA damage response (DDR) is a key pathway for tissue degeneration and organismal aging; however, the precise protective role of DDR in stem cell/niche aging is unclear. The Drosophila midgut is an excellent model to study the biology of stem cell/niche aging because of its easy genetic manipulation and its short lifespan. Here, we showed that deficiency of DDR in Drosophila enterocytes (ECs) accelerates intestinal stem cell (ISC) aging. We generated flies with knockdown of Mre11, Rad50, Nbs1, ATM, ATR, Chk1, and Chk2, which decrease the DDR system in ECs. EC-specific DDR depletion induced EC death, accelerated the aging of ISCs, as evidenced by ISC hyperproliferation, DNA damage accumulation, and increased centrosome amplification, and affected the adult fly’s survival. Our data indicated a distinct effect of DDR depletion in stem or niche cells on tissue-resident stem cell proliferation. Our findings provide evidence of the essential role of DDR in protecting EC against ISC aging, thus providing a better understanding of the molecular mechanisms of stem cell/niche aging.
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Methylomic survival predictors, frailty, and mortality

Yan Zhang, Kai-Uwe Saum, Ben Schöttker, Bernd Holleczek, Hermann Brenner,

https://doi.org/10.18632/aging.101392 pp 339—357

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Zhang Y, Saum K, Schöttker B, Holleczek B, Brenner H, . Methylomic survival predictors, frailty, and mortality. . 10:339-357. https://doi.org/10.18632/aging.101392

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                TY  - JOUR
                AU  - Zhang, Yan 
                AU  - Saum, Kai-Uwe 
                AU  - Schöttker, Ben 
                AU  - Holleczek, Bernd 
                AU  - Brenner, Hermann 
                TI  - Methylomic survival predictors, frailty, and mortality
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101392
                DO  - 10.18632/aging.101392
                SP  - 339
                EP  - 357
                PY  - 
                AB  - Survival predictors are of potential use for informing on biological age and targeting prevention of aging-related morbidity. We assessed associations of 2 novel methylomic survival indicators, a methylation-based mortality risk score (MRscore) and the epigenetic clock-derived age acceleration (AA), with a well-known survival predictor, frailty index (FI), and compared the 3 indicators in mortality prediction. In a large population-based cohort with 14-year follow-up, we found both MRscore and AA to be independently associated with FI, but the association was much stronger for MRscore than for AA. Although all 3 indicators were individually associated with all-cause mortality, robust associations only persisted for MRscore and FI when simultaneously including the 3 indicators in regression models, with hazard ratios (95% CI) of 1.91 (1.63–2.22), 1.37 (1.25–1.51), and 1.05 (0.90–1.22), respectively, per standard deviation increase of MRscore, FI, and AA. Prediction error curves, Harrell’s C-statistics, and time-dependent AUCs all showed higher predictive accuracy for MRscore than for FI and AA. These findings were validated in independent samples. Our study demonstrates the ability of the MRscore to strongly enhance survival prediction beyond established markers of biological age, such as FI and AA, and it thus bears potential of a surrogate endpoint for clinical research and intervention.
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Intestinal immunity in hypopituitary dwarf mice: effects of age

Xin Wang, Justin Darcy, Chuan Cai, Junfei Jin, Andrzej Bartke, Deliang Cao,

https://doi.org/10.18632/aging.101393 pp 358—370

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Wang X, Darcy J, Cai C, Jin J, Bartke A, Cao D, . Intestinal immunity in hypopituitary dwarf mice: effects of age. . 10:358-370. https://doi.org/10.18632/aging.101393

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                TY  - JOUR
                AU  - Wang, Xin 
                AU  - Darcy, Justin 
                AU  - Cai, Chuan 
                AU  - Jin, Junfei 
                AU  - Bartke, Andrzej 
                AU  - Cao, Deliang 
                TI  - Intestinal immunity in hypopituitary dwarf mice: effects of age
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101393
                DO  - 10.18632/aging.101393
                SP  - 358
                EP  - 370
                PY  - 
                AB  - Hypopituitary dwarf mice demonstrate advantages of longevity, but little is known of their colon development and intestinal immunity. Herein we found that Ames dwarf mice have shorter colon and colonic crypts, but larger ratio of mesenteric lymph nodes (MLNs) over body weight than age-matched wild type (WT) mice. In the colonic lamina propria (cLP) of juvenile Ames mice, more inflammatory neutrophils (Ā: 0.15% vs. 0.03% in WT mice) and monocytes (Ā: 7.97% vs. 5.15%) infiltrated, and antigen presenting cells CD11c+ dendritic cells (Ā: 1.39% vs. 0.87%), CD11b+ macrophages (Ā: 3.22% vs. 0.81%) and gamma delta T (γδ T) cells (Ā: 5.56% vs. 1.35%) were increased. In adult Ames dwarf mice, adaptive immune cells, such as IL-17 producing CD4+ T helper (Th17) cells (Ā: 8.3% vs. 4.7%) were augmented. In the MLNs of Ames dwarf mice, the antigen presenting and adaptive immune cells also altered when compared to WT mice, such as a decrease of T-regulatory (Treg) cells in juvenile Ames mice (Ā: 7.7% vs.10.5%), but an increase of Th17 cells (Ā: 0.627% vs.0.093%). Taken together, these data suggest that somatotropic signaling deficiency influences colon development and intestinal immunity.
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CD40L promotes development of acute aortic dissection via induction of inflammation and impairment of endothelial cell function

Lu Han, Lu Dai, Yuan-Fei Zhao, Hai-Yang Li, Ou Liu, Feng Lan, Wen-Jian Jiang, Hong-Jia Zhang,

https://doi.org/10.18632/aging.101394 pp 371—385

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Han L, Dai L, Zhao Y, Li H, Liu O, Lan F, Jiang W, Zhang H, . CD40L promotes development of acute aortic dissection via induction of inflammation and impairment of endothelial cell function. . 10:371-385. https://doi.org/10.18632/aging.101394

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                TY  - JOUR
                AU  - Han, Lu 
                AU  - Dai, Lu 
                AU  - Zhao, Yuan-Fei 
                AU  - Li, Hai-Yang 
                AU  - Liu, Ou 
                AU  - Lan, Feng 
                AU  - Jiang, Wen-Jian 
                AU  - Zhang, Hong-Jia 
                TI  - CD40L promotes development of acute aortic dissection via induction of inflammation and impairment of endothelial cell function
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101394
                DO  - 10.18632/aging.101394
                SP  - 371
                EP  - 385
                PY  - 
                AB  - Acute aortic dissection is one of the most lethal cardiovascular disease. The major histopathological feature of AAD is medial degradation, especially breakdown of elastin and collagen. However, the underlying mechanism remains a mystery. Platelets expressed CD40 Ligand (CD40L) is recently recognised as a key effector of cardiovascular disease development through its pro-inflammatory effect. To clarify the role of CD40L in AAD, we examined level of CD40L in human blood serum samples and found that it is significantly higher in AAD patients compared with healthy subjects (26.8±5.52 ng/mL versus 13.4±4.00 ng/mL). To further investigate if CD40L is involve in the development of AAD, we applied β-aminopropionitrile (BAPN) induced mouse model of AAD. Consistent with the human data, circulating CD40L in AAD mice much higher than normal mice (148.40±75.96 pg/mL versus 44.09±19.65 pg/mL). Meanwhile, multiple pro-inflammatory chemokines significantly increased in AAD mice. Importantly, the CD40L-/- mice treated with BAPN did not develop these phenotypes. Lastly, we confirmed that endothelial cells migration was significantly inhibited by CD40L, suggesting impaired recovery from intimal injury. In summary, we found that CD40L promoted AAD development through its pro-inflammatory effects and inhibition of endothelial cell function.
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Metformin reduces glucose intolerance caused by rapamycin treatment in genetically heterogeneous female mice

Roxanne Weiss, Elizabeth Fernandez, Yuhong Liu, Randy Strong, Adam B. Salmon,

https://doi.org/10.18632/aging.101401 pp 386—401

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Weiss R, Fernandez E, Liu Y, Strong R, Salmon AB, . Metformin reduces glucose intolerance caused by rapamycin treatment in genetically heterogeneous female mice. . 10:386-401. https://doi.org/10.18632/aging.101401

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                TY  - JOUR
                AU  - Weiss, Roxanne 
                AU  - Fernandez, Elizabeth 
                AU  - Liu, Yuhong 
                AU  - Strong, Randy 
                AU  - Salmon, Adam B. 
                TI  - Metformin reduces glucose intolerance caused by rapamycin treatment in genetically heterogeneous female mice
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101401
                DO  - 10.18632/aging.101401
                SP  - 386
                EP  - 401
                PY  - 
                AB  - The use of rapamycin to extend lifespan and delay age-related disease in mice is well-established despite its potential to impair glucose metabolism which is driven partially due to increased hepatic gluconeogenesis. We tested whether a combination therapeutic approach using rapamycin and metformin could diminish some of the known metabolic defects caused by rapamycin treatment in mice. In genetically heterogeneous HET3 mice, we found that chronic administration of encapsulated rapamycin by diet caused a measurable defect in glucose metabolism in both male and female mice as early as 1 month after treatment. In female mice, this defect was alleviated over time by simultaneous treatment with metformin, also by diet, such that females treated with both drugs where indistinguishable from control mice during glucose tolerance tests. While rapamycin-mediated glucose intolerance was unaffected by metformin in males, we found metformin prevented rapamycin-mediated reduction in insulin and leptin concentrations following 9 months of co-treatment. Recently, the Interventions Testing Program showed that mice treated with metformin and rapamycin live at least as long as those treated with rapamycin alone. Together, our data provide compelling evidence that the pro-longevity effects of rapamycin can be uncoupled from its detrimental effects on metabolism through combined therapeutic approaches.
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Preferential Ty1 retromobility in mother cells and nonquiescent stationary phase cells is associated with increased concentrations of total Gag or processed Gag and is inhibited by exposure to a high concentration of calcium

Andrew C. Peifer, Patrick H. Maxwell,

https://doi.org/10.18632/aging.101402 pp 402—424

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Peifer AC, Maxwell PH, . Preferential Ty1 retromobility in mother cells and nonquiescent stationary phase cells is associated with increased concentrations of total Gag or processed Gag and is inhibited by exposure to a high concentration of calcium. . 10:402-424. https://doi.org/10.18632/aging.101402

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                TY  - JOUR
                AU  - Peifer, Andrew C. 
                AU  - Maxwell, Patrick H. 
                TI  - Preferential Ty1 retromobility in mother cells and nonquiescent stationary phase cells is associated with increased concentrations of total Gag or processed Gag and is inhibited by exposure to a high concentration of calcium
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101402
                DO  - 10.18632/aging.101402
                SP  - 402
                EP  - 424
                PY  - 
                AB  - Retrotransposons are abundant mobile DNA elements in eukaryotic genomes that are more active with age in diverse species. Details of the regulation and consequences of retrotransposon activity during aging remain to be determined. Ty1 retromobility in Saccharomyces cerevisiae is more frequent in mother cells compared to daughter cells, and we found that Ty1 was more mobile in nonquiescent compared to quiescent subpopulations of stationary phase cells. This retromobility asymmetry was absent in mutant strains lacking BRP1 that have reduced expression of the essential Pma1p plasma membrane proton pump, lacking the mRNA decay gene LSM1, and in cells exposed to a high concentration of calcium. Mother cells had higher levels of Ty1 Gag protein than daughters. The proportion of protease-processed Gag decreased as cells transitioned to stationary phase, processed Gag was the dominant form in nonquiescent cells, but was virtually absent from quiescent cells. Treatment with calcium reduced total Gag levels and the proportion of processed Gag, particularly in mother cells. We also found that Ty1 reduced the fitness of proliferating but not stationary phase cells. These findings may be relevant to understanding regulation and consequences of retrotransposons during aging in other organisms, due to conserved impacts and regulation of retrotransposons.
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Can Serum Cystatin C predict long-term survival in cardiac surgery patients?

Valentina Rovella, Giulia Marrone, Mariarita Dessì, Michele Ferrannini, Nicola Toschi, Antonio Pellegrino, Maurizio Casasco, Nicola Di Daniele, Annalisa Noce,

https://doi.org/10.18632/aging.101403 pp 425—433

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Rovella V, Marrone G, Dessì M, Ferrannini M, Toschi N, Pellegrino A, Casasco M, Di Daniele N, Noce A, . Can Serum Cystatin C predict long-term survival in cardiac surgery patients?. . 10:425-433. https://doi.org/10.18632/aging.101403

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                TY  - JOUR
                AU  - Rovella, Valentina 
                AU  - Marrone, Giulia 
                AU  - Dessì, Mariarita 
                AU  - Ferrannini, Michele 
                AU  - Toschi, Nicola 
                AU  - Pellegrino, Antonio 
                AU  - Casasco, Maurizio 
                AU  - Di Daniele, Nicola 
                AU  - Noce, Annalisa 
                TI  - Can Serum Cystatin C predict long-term survival in cardiac surgery patients?
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101403
                DO  - 10.18632/aging.101403
                SP  - 425
                EP  - 433
                PY  - 
                AB  - Renal dysfunction is a risk factor for morbidity and mortality in cardiac surgery patients. Serum Cystatin C (sCysC) is a well-recognized marker of early renal dysfunction but few reports evaluate its prognostic cardio-vascular role. The aim of the study is to consider the prognostic value of sCysC for cardiovascular mortality. Four hundred twenty-four cardiac-surgery patients (264 men and 160 women) were enrolled. At admission, all patients were tested for renal function and inflammatory status. Patients were subdivided in subgroups according to the values of the following variables: sCysC, serum Creatinine (sCrea), age, high sensitivity-C Reactive Protein, fibrinogen, surgical procedures and Kaplan-Meier cumulative survival curves were plotted. The primary end-point was cardiovascular mortality. In order to evaluate the simultaneous independent impact of all measured variables on survival we fitted a multivariate Cox-Proportional Hazard Model (CPHM). In Kaplan-Meier analysis 124 patients (29.4%) reached the end-point. In multivariate CPHM, the only significant predictors of mortality were sCysC (p&lt;0.00001, risk ratio: 1.529, CI: 1.29-1.80) and age (p=0.039, risk ratio: 1.019, CI: 1.001-1.037). When replacing sCysC with sCrea, the only significant predictor of mortality was sCrea (p=0.0026; risk ratio 1.20; CI: 1.06-1.36). Increased levels of sCysC can be considered a useful biomarker of cardiovascular mortality in cardiac-surgery patients.
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Induction, regulation and roles of neural adhesion molecule L1CAM in cellular senescence

Blanka Mrazkova, Rastislav Dzijak, Terezie Imrichova, Lenka Kyjacova, Peter Barath, Petr Dzubak, Dusan Holub, Marian Hajduch, Zuzana Nahacka, Ladislav Andera, Petr Holicek, Pavla Vasicova, Olena Sapega, Jiri Bartek, Zdenek Hodny,

https://doi.org/10.18632/aging.101404 pp 434—462

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Mrazkova B, Dzijak R, Imrichova T, Kyjacova L, Barath P, Dzubak P, Holub D, Hajduch M, Nahacka Z, Andera L, Holicek P, Vasicova P, Sapega O, et al, . Induction, regulation and roles of neural adhesion molecule L1CAM in cellular senescence. . 10:434-462. https://doi.org/10.18632/aging.101404

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                TY  - JOUR
                AU  - Mrazkova, Blanka 
                AU  - Dzijak, Rastislav 
                AU  - Imrichova, Terezie 
                AU  - Kyjacova, Lenka 
                AU  - Barath, Peter 
                AU  - Dzubak, Petr 
                AU  - Holub, Dusan 
                AU  - Hajduch, Marian 
                AU  - Nahacka, Zuzana 
                AU  - Andera, Ladislav 
                AU  - Holicek, Petr 
                AU  - Vasicova, Pavla 
                AU  - Sapega, Olena 
                AU  - Bartek, Jiri 
                AU  - Hodny, Zdenek 
                TI  - Induction, regulation and roles of neural adhesion molecule L1CAM in cellular senescence
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101404
                DO  - 10.18632/aging.101404
                SP  - 434
                EP  - 462
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Mrazkova, Blanka 
                AU  - Dzijak, Rastislav 
                AU  - Imrichova, Terezie 
                AU  - Kyjacova, Lenka 
                AU  - Barath, Peter 
                AU  - Dzubak, Petr 
                AU  - Holub, Dusan 
                AU  - Hajduch, Marian 
                AU  - Nahacka, Zuzana 
                AU  - Andera, Ladislav 
                AU  - Holicek, Petr 
                AU  - Vasicova, Pavla 
                AU  - Sapega, Olena 
                AU  - Bartek, Jiri 
                AU  - Hodny, Zdenek 
                TI  - Induction, regulation and roles of neural adhesion molecule L1CAM in cellular senescence
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101404
                DO  - 10.18632/aging.101404
                SP  - 434
                EP  - 462
                PY  - 
                AB  - Aging involves tissue accumulation of senescent cells (SC) whose elimination through senolytic approaches may evoke organismal rejuvenation. SC also contribute to aging-associated pathologies including cancer, hence it is imperative to better identify and target SC. Here, we aimed to identify new cell-surface proteins differentially expressed on human SC. Besides previously reported proteins enriched on SC, we identified 78 proteins enriched and 73 proteins underrepresented in replicatively senescent BJ fibroblasts, including L1CAM, whose expression is normally restricted to the neural system and kidneys. L1CAM was: 1) induced in premature forms of cellular senescence triggered chemically and by gamma-radiation, but not in Ras-induced senescence; 2) induced upon inhibition of cyclin-dependent kinases by p16INK4a; 3) induced by TGFbeta and suppressed by RAS/MAPK(Erk) signaling (the latter explaining the lack of L1CAM induction in RAS-induced senescence); and 4) induced upon downregulation of growth-associated gene ANT2, growth in low-glucose medium or inhibition of the mevalonate pathway. These data indicate that L1CAM is controlled by a number of cell growth- and metabolism-related pathways during SC development. Functionally, SC with enhanced surface L1CAM showed increased adhesion to extracellular matrix and migrated faster. Our results provide mechanistic insights into senescence of human cells, with implications for future senolytic strategies.
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Protective effects of melatonin against nicotine-induced disorder of mouse early folliculogenesis

Yu-Feng Wang, Xiao-Feng Sun, Ze-Li Han, Lan Li, Wei Ge, Yong Zhao, Massimo De Felici, Wei Shen, Shun-Feng Cheng,

https://doi.org/10.18632/aging.101405 pp 463—480

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Wang Y, Sun X, Han Z, Li L, Ge W, Zhao Y, De Felici M, Shen W, Cheng S, . Protective effects of melatonin against nicotine-induced disorder of mouse early folliculogenesis. . 10:463-480. https://doi.org/10.18632/aging.101405

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                TY  - JOUR
                AU  - Wang, Yu-Feng 
                AU  - Sun, Xiao-Feng 
                AU  - Han, Ze-Li 
                AU  - Li, Lan 
                AU  - Ge, Wei 
                AU  - Zhao, Yong 
                AU  - De Felici, Massimo 
                AU  - Shen, Wei 
                AU  - Cheng, Shun-Feng 
                TI  - Protective effects of melatonin against nicotine-induced disorder of mouse early folliculogenesis
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101405
                DO  - 10.18632/aging.101405
                SP  - 463
                EP  - 480
                PY  - 
                AB  - In this paper, we show that neonatal mice injected for five consecutive days with nicotine display impaired germ cell cyst breakdown and primordial follicle assembly resulting in decreased ovarian reserve lasting until sex maturation age. The effects of nicotine on the pups ovaries were associated with decreased expression of oocyte specific genes such as Nobox, Lhx8, Figlα and Sohlh2. Moreover, the ovaries of pups injected with nicotine showed increased level of cell oxidative stress and autophagic markers (upregulation of AMPKα-1, increased ratio LC3-II/LC3-I, downregulation of AKT and mTOR). Noteworthy, all these effects were counteracted by the administration of the hormone melatonin in 1 μM. In vitro culture of 0 dpp ovaries for 5 days in the presence of 10 μM nicotine reproduced its effect on germ cell cyst breakdown and primordial follicle assembly, furthermore it also revealing about 20% reduction of somatic cells proliferation, and these effects was prevented when melatonin was added to the medium. Taken together these results show that nicotine exposure can adversely affect the establishment of the ovarian reserve in the mouse likely by locally inducing cellular stress altering the primordial follicle assembly and that melatonin, however, is able to counteract such effects.
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Associations between lncRNA MEG3 polymorphisms and neuroblastoma risk in Chinese children

Zhen-Jian Zhuo, Ruizhong Zhang, Jiao Zhang, Jinhong Zhu, Tianyou Yang, Yan Zou, Jing He, Huimin Xia,

https://doi.org/10.18632/aging.101406 pp 481—491

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Zhuo Z, Zhang R, Zhang J, Zhu J, Yang T, Zou Y, He J, Xia H, . Associations between lncRNA MEG3 polymorphisms and neuroblastoma risk in Chinese children. . 10:481-491. https://doi.org/10.18632/aging.101406

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                TY  - JOUR
                AU  - Zhuo, Zhen-Jian 
                AU  - Zhang, Ruizhong 
                AU  - Zhang, Jiao 
                AU  - Zhu, Jinhong 
                AU  - Yang, Tianyou 
                AU  - Zou, Yan 
                AU  - He, Jing 
                AU  - Xia, Huimin 
                TI  - Associations between lncRNA<i> MEG3</i> polymorphisms and neuroblastoma risk in Chinese children
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101406
                DO  - 10.18632/aging.101406
                SP  - 481
                EP  - 491
                PY  - 
                AB  - Neuroblastoma is the third most common childhood cancer after leukemias and cancer of the central nervous system. Long noncoding RNA MEG3 polymorphisms have been shown to confer cancer susceptibility; however, their roles in the genetic predisposition to neuroblastoma remain unclarified. To answer this question, we genotyped two MEG3 polymorphisms, rs7158663 G&gt;A and rs4081134 G&gt;A, in 392 neuroblastoma children and 783 controls by TaqMan method. The results showed that neither single locus nor the combination analysis supported an association between MEG3 polymorphism and neuroblastoma risk. Interestingly, we found that subjects carrying rs4081134 AG/AA genotypes significantly tended to develop neuroblastoma among subgroups with age &gt;18 month (adjusted OR=1.36, 95% CI=1.01-1.84) and clinical stage III+IV disease (adjusted OR=1.47, 95% CI=1.08-1.99), when compared with reference group. In the combined analysis of MEG3 polymorphisms, we found that carriers of 2 risk genotypes were more likely to have higher risk of developing neuroblastoma than those with 0-1 risk genotype among children more than 18 months of age (adjusted OR=1.36, 95% CI=1.01-1.84, P=0.042), and with clinical stages III+IV disease (adjusted OR=1.47, 95% CI=1.08-2.00, P=0.014). Our data suggest MEG3 as a weak-effect neuroblastoma susceptibility gene. Well-designed studies with large sample studies are needed to further validate this finding.
                ER  -

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Strong impact of natural-selection–free heterogeneity in genetics of age-related phenotypes

Alexander M. Kulminski, Jian Huang, Yury Loika, Konstantin G. Arbeev, Olivia Bagley, Arseniy Yashkin, Matt Duan, Irina Culminskaya,

https://doi.org/10.18632/aging.101407 pp 492—514

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Kulminski AM, Huang J, Loika Y, Arbeev KG, Bagley O, Yashkin A, Duan M, Culminskaya I, . Strong impact of natural-selection–free heterogeneity in genetics of age-related phenotypes. . 10:492-514. https://doi.org/10.18632/aging.101407

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                TY  - JOUR
                AU  - Kulminski, Alexander M. 
                AU  - Huang, Jian 
                AU  - Loika, Yury 
                AU  - Arbeev, Konstantin G. 
                AU  - Bagley, Olivia 
                AU  - Yashkin, Arseniy 
                AU  - Duan, Matt 
                AU  - Culminskaya, Irina 
                TI  - Strong impact of natural-selection–free heterogeneity in genetics of age-related phenotypes
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101407
                DO  - 10.18632/aging.101407
                SP  - 492
                EP  - 514
                PY  - 
                AB  - A conceptual difficulty in genetics of age-related phenotypes that make individuals vulnerable to disease in post-reproductive life is genetic heterogeneity attributed to an undefined role of evolution in establishing their molecular mechanisms. Here, we performed univariate and pleiotropic genome-wide meta-analyses of 20 age-related phenotypes leveraging longitudinal information in a sample of 33,431 individuals and dealing with the natural-selection–free genetic heterogeneity. We identified 142 non-proxy single nucleotide polymorphisms (SNPs) with phenotype-specific (18 SNPs) and pleiotropic (124 SNPs) associations at genome-wide level. Univariate meta-analysis identified two novel (11.1%) and replicated 16 SNPs whereas pleiotropic meta-analysis identified 115 novel (92.7%) and nine replicated SNPs. Pleiotropic associations for most novel (93.9%) and all replicated SNPs were strongly impacted by the natural-selection–free genetic heterogeneity in its unconventional form of antagonistic heterogeneity, implying antagonistic directions of genetic effects for directly correlated phenotypes. Our results show that the common genome-wide approach is well adapted to handle homogeneous univariate associations within Mendelian framework whereas most associations with age-related phenotypes are more complex and well beyond that framework. Dissecting the natural-selection–free genetic heterogeneity is critical for gaining insights into genetics of age-related phenotypes and has substantial and unexplored yet potential for improving efficiency of genome-wide analysis.
                ER  -

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Correction: Identification of new genetic variants of HLA-DQB1 associated with human longevity and lipid homeostasis—a cross-sectional study in a Chinese population

Fan Yang, Liang Sun, Xiaoquan Zhu, Jing Han, Yi Zeng, Chao Nie, Huiping Yuan, Xiaoling Li, Xiaohong Shi, Yige Yang, Caiyou Hu, Zeping Lv, Zezhi Huang, Chenguang Zheng, Siying Liang, Jin Huang, Gang Wan, Keyan Qi, Bin Qin, Suyan Cao, Xin Zhao, Yongqiang Zhang, Ze Yang,

https://doi.org/10.18632/aging.101400 pp 515

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Yang F, Sun L, Zhu X, Han J, Zeng Y, Nie C, Yuan H, Li X, Shi X, Yang Y, Hu C, Lv Z, Huang Z, et al, . Correction: Identification of new genetic variants of HLA-DQB1 associated with human longevity and lipid homeostasis—a cross-sectional study in a Chinese population. . 10:515-515. https://doi.org/10.18632/aging.101400

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                TY  - JOUR
                AU  - Yang, Fan 
                AU  - Sun, Liang 
                AU  - Zhu, Xiaoquan 
                AU  - Han, Jing 
                AU  - Zeng, Yi 
                AU  - Nie, Chao 
                AU  - Yuan, Huiping 
                AU  - Li, Xiaoling 
                AU  - Shi, Xiaohong 
                AU  - Yang, Yige 
                AU  - Hu, Caiyou 
                AU  - Lv, Zeping 
                AU  - Huang, Zezhi 
                AU  - Zheng, Chenguang 
                AU  - Liang, Siying 
                AU  - Huang, Jin 
                AU  - Wan, Gang 
                AU  - Qi, Keyan 
                AU  - Qin, Bin 
                AU  - Cao, Suyan 
                AU  - Zhao, Xin 
                AU  - Zhang, Yongqiang 
                AU  - Yang, Ze 
                TI  - Correction: Identification of new genetic variants of HLA-DQB1 associated with human longevity and lipid homeostasis—a cross-sectional study in a Chinese population
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101400
                DO  - 10.18632/aging.101400
                SP  - 515
                EP  - 515
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yang, Fan 
                AU  - Sun, Liang 
                AU  - Zhu, Xiaoquan 
                AU  - Han, Jing 
                AU  - Zeng, Yi 
                AU  - Nie, Chao 
                AU  - Yuan, Huiping 
                AU  - Li, Xiaoling 
                AU  - Shi, Xiaohong 
                AU  - Yang, Yige 
                AU  - Hu, Caiyou 
                AU  - Lv, Zeping 
                AU  - Huang, Zezhi 
                AU  - Zheng, Chenguang 
                AU  - Liang, Siying 
                AU  - Huang, Jin 
                AU  - Wan, Gang 
                AU  - Qi, Keyan 
                AU  - Qin, Bin 
                AU  - Cao, Suyan 
                AU  - Zhao, Xin 
                AU  - Zhang, Yongqiang 
                AU  - Yang, Ze 
                TI  - Correction: Identification of new genetic variants of HLA-DQB1 associated with human longevity and lipid homeostasis—a cross-sectional study in a Chinese population
                JO  - 
                JA  - 
                VL  - 10
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101400
                DO  - 10.18632/aging.101400
                SP  - 515
                EP  - 515
                PY  - 
                AB  - 
                ER  -

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Volume 10, Issue 3

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Editorials

Stefan Kaluz, Chalet Tan, Erwin G. Van Meir,

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Michael Garratt, Michael B. Stout,

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Stéphane Fourcade, Tiago F. Outeiro, Aurora Pujol,

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Zhonghe Ke, Andrei Seluanov, Vera Gorbunova,

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Eleni Petsalaki, George Zachos,

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Timothy E. Hoffman, Lyle E. Wallis, William H. Hanneman,

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A.M.P.B. Seneviratne, Geri Kreitzer,

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Review

Yu-Lan Chu, Ya-Ru Xu, Wan-Xi Yang, Yi Sun,

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Research Papers

Joung-Sun Park, Ho-Jun Jeon, Jung-Hoon Pyo, Young-Shin Kim, Mi-Ae Yoo,

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Yan Zhang, Kai-Uwe Saum, Ben Schöttker, Bernd Holleczek, Hermann Brenner,

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Xin Wang, Justin Darcy, Chuan Cai, Junfei Jin, Andrzej Bartke, Deliang Cao,

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Lu Han, Lu Dai, Yuan-Fei Zhao, Hai-Yang Li, Ou Liu, Feng Lan, Wen-Jian Jiang, Hong-Jia Zhang,

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Roxanne Weiss, Elizabeth Fernandez, Yuhong Liu, Randy Strong, Adam B. Salmon,

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Andrew C. Peifer, Patrick H. Maxwell,

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Valentina Rovella, Giulia Marrone, Mariarita Dessì, Michele Ferrannini, Nicola Toschi, Antonio Pellegrino, Maurizio Casasco, Nicola Di Daniele, Annalisa Noce,

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Blanka Mrazkova, Rastislav Dzijak, Terezie Imrichova, Lenka Kyjacova, Peter Barath, Petr Dzubak, Dusan Holub, Marian Hajduch, Zuzana Nahacka, Ladislav Andera, Petr Holicek, Pavla Vasicova, Olena Sapega, Jiri Bartek, Zdenek Hodny,

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Yu-Feng Wang, Xiao-Feng Sun, Ze-Li Han, Lan Li, Wei Ge, Yong Zhao, Massimo De Felici, Wei Shen, Shun-Feng Cheng,

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Zhen-Jian Zhuo, Ruizhong Zhang, Jiao Zhang, Jinhong Zhu, Tianyou Yang, Yan Zou, Jing He, Huimin Xia,

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Alexander M. Kulminski, Jian Huang, Yury Loika, Konstantin G. Arbeev, Olivia Bagley, Arseniy Yashkin, Matt Duan, Irina Culminskaya,

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