Volume 3, Issue 4

Menendez JA, Cufí S, Oliveras-Ferraros C, Vellon L, Joven J, Vazquez-Martin A, . Gerosuppressant Metformin: less is more. . 3:348-362. https://doi.org/10.18632/aging.100316

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Insights from model organisms on the functions of the tumor suppressor protein LKB1: Zebrafish chips in

Yme U. van der Velden, Anna-Pavlina G. Haramis,

https://doi.org/10.18632/aging.100319 pp 363—367

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van der Velden YU, Haramis AG, . Insights from model organisms on the functions of the tumor suppressor protein LKB1: Zebrafish chips in. . 3:363-367. https://doi.org/10.18632/aging.100319

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Association of PTPN22 1858T/T genotype with type 1 diabetes, Graves' disease but not with rheumatoid arthritis in Russian population

Daria Zhebrun, Yulia Kudryashova, Alina Babenko, Alexei Maslyansky, Natalya Kunitskaya, Daria Popcova, Alexandra Klushina, Elena Grineva, Anna Kostareva, Evgeny Shlyakhto,

https://doi.org/10.18632/aging.100305 pp 368—373

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Zhebrun D, Kudryashova Y, Babenko A, Maslyansky A, Kunitskaya N, Popcova D, Klushina A, Grineva E, Kostareva A, Shlyakhto E, . Association of PTPN22 1858T/T genotype with type 1 diabetes, Graves' disease but not with rheumatoid arthritis in Russian population. . 3:368-373. https://doi.org/10.18632/aging.100305

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                TY  - JOUR
                AU  - Zhebrun, Daria 
                AU  - Kudryashova, Yulia 
                AU  - Babenko, Alina 
                AU  - Maslyansky, Alexei 
                AU  - Kunitskaya, Natalya 
                AU  - Popcova, Daria 
                AU  - Klushina, Alexandra 
                AU  - Grineva, Elena 
                AU  - Kostareva, Anna 
                AU  - Shlyakhto, Evgeny 
                TI  - Association of PTPN22 1858T/T genotype with type 1 diabetes, Graves' disease but not with rheumatoid arthritis in Russian population
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100305
                DO  - 10.18632/aging.100305
                SP  - 368
                EP  - 373
                PY  - 
                AB  - The protein tyrosine phosphatase nonreceptor 22 gene (PTPN22) is an important negative regulator of signal transduction through the T-cell receptors (TCR). Recently a single-nucleotide polymorphism (SNP) 1858 C/T within this gene was shown to be a risk factor for several autoimmune diseases, such as rheumatoid arthritis (RA), Graves' Disease (GD), systemic lupus erythematosus (SLE), Wegener's granulomatosis (WG) and type 1 diabetes mellitus (T1D). The aim of this study was to analyze a possible association between 1858 C/T SNP and a number of autoimmune diseases, including RA, GD and T1D in Russian population. Patients with T1D, GD, RA and healthy controls were genotyped for the 1858 C/T SNP in PTPN22 gene. We found a significant association between PTPN22 1858 C/T SNP and T1D and GD. 1858T/T genotype was observed more frequently in T1D and GD patients compared to control subjects. No such association was observed for RA. In concordance with a previous data establishing PTPN22 1858 C/T SNP association with several autoimmune diseases, our findings provide further evidence that the PTPN22 gene may play an important role in the susceptibility to some autoimmune diseases.
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Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans

Andreea Soare, Roberto Cangemi, Daniela Omodei, John O. Holloszy, Luigi Fontana,

https://doi.org/10.18632/aging.100280 pp 374—379

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Soare A, Cangemi R, Omodei D, Holloszy JO, Fontana L, . Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans. . 3:374-379. https://doi.org/10.18632/aging.100280

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                TY  - JOUR
                AU  - Soare, Andreea 
                AU  - Cangemi, Roberto 
                AU  - Omodei, Daniela 
                AU  - Holloszy, John O. 
                AU  - Fontana, Luigi 
                TI  - Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100280
                DO  - 10.18632/aging.100280
                SP  - 374
                EP  - 379
                PY  - 
                AB  - Reduction of body temperature has been proposed to contribute to the increased lifespan in calorie restricted animals and mice overexpressing the uncoupling protein-2 in hypocretin neurons. However, nothing is known regarding the long-term effects of calorie restriction (CR) with adequate nutrition on body temperature in humans. In this study, 24-hour core body temperature was measured every minute by using ingested telemetric capsules in 24 men and women (mean age 53.7±9.4 yrs) consuming a CR diet for an average of 6 years, 24 age- and sex-matched sedentary (WD) and 24 body fat-matched exercise-trained (EX) volunteers, who were eating Western diets. The CR and EX groups were significantly leaner than the WD group. Energy intake was lower in the CR group (1769±348 kcal/d) than in the WD (2302±668 kcal/d) and EX (2798±760 kcal/d) groups (P&lt;0.0001). Mean 24-hour, day-time and night-time core body temperatures were all significantly lower in the CR group than in the WD and EX groups (P≤0.01). Long-term CR with adequate nutrition in lean and weight-stable healthy humans is associated with a sustained reduction in core body temperature, similar to that found in CR rodents and monkeys. This adaptation is likely due to CR itself, rather than to leanness, and may be involved in slowing the rate of aging.
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Generation of induced pluripotent stem cell lines from 3 distinct laminopathies bearing heterogeneous mutations in lamin A/C

Jenny CY Ho, Ting Zhou, Wing-Hon Lai, Yinghua Huang, Yau-Chi Chan, Xingyan Li, Navy LY Wong, Yanhua Li, Ka-Wing Au, Dongsheng Guo, Jianyong Xu, Chung-Wah Siu, Duanqing Pei, Hung-Fat Tse, Miguel Angel Esteban,

https://doi.org/10.18632/aging.100277 pp 380—390

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Ho JC, Zhou T, Lai W, Huang Y, Chan Y, Li X, Wong NL, Li Y, Au K, Guo D, Xu J, Siu C, Pei D, et al, . Generation of induced pluripotent stem cell lines from 3 distinct laminopathies bearing heterogeneous mutations in lamin A/C. . 3:380-390. https://doi.org/10.18632/aging.100277

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                TY  - JOUR
                AU  - Ho, Jenny CY 
                AU  - Zhou, Ting 
                AU  - Lai, Wing-Hon 
                AU  - Huang, Yinghua 
                AU  - Chan, Yau-Chi 
                AU  - Li, Xingyan 
                AU  - Wong, Navy LY 
                AU  - Li, Yanhua 
                AU  - Au, Ka-Wing 
                AU  - Guo, Dongsheng 
                AU  - Xu, Jianyong 
                AU  - Siu, Chung-Wah 
                AU  - Pei, Duanqing 
                AU  - Tse, Hung-Fat 
                AU  - Esteban, Miguel Angel 
                TI  - Generation of induced pluripotent stem cell lines from 3 distinct laminopathies bearing heterogeneous mutations in lamin A/C
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100277
                DO  - 10.18632/aging.100277
                SP  - 380
                EP  - 390
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ho, Jenny CY 
                AU  - Zhou, Ting 
                AU  - Lai, Wing-Hon 
                AU  - Huang, Yinghua 
                AU  - Chan, Yau-Chi 
                AU  - Li, Xingyan 
                AU  - Wong, Navy LY 
                AU  - Li, Yanhua 
                AU  - Au, Ka-Wing 
                AU  - Guo, Dongsheng 
                AU  - Xu, Jianyong 
                AU  - Siu, Chung-Wah 
                AU  - Pei, Duanqing 
                AU  - Tse, Hung-Fat 
                AU  - Esteban, Miguel Angel 
                TI  - Generation of induced pluripotent stem cell lines from 3 distinct laminopathies bearing heterogeneous mutations in lamin A/C
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100277
                DO  - 10.18632/aging.100277
                SP  - 380
                EP  - 390
                PY  - 
                AB  - The term laminopathies defines a group of genetic disorders caused by defects in the nuclear envelope, mostly the lamins. Lamins are the main constituents of the nuclear lamina, a filamentous meshwork associated with the inner nuclear membrane that provides mechanical stability and plays important roles in processes such as transcription, DNA replication and chromatin organization. More than 300 mutations in lamin A/C have been associated with diverse clinical phenotypes, understanding the molecular basis of these diseases may provide a rationale for treating them. Here we describe the generation of induced pluripotent stem cells (iPSCs) from a patient with inherited dilated cardiomiopathy and 2 patients with distinct accelerated forms of aging, atypical Werner syndrome and Hutchinson Gilford progeria, all of which are caused by mutations in lamin A/C. These cell lines were pluripotent and displayed normal nuclear membrane morphology compared to donor fibroblasts. Their differentiated progeny reproduced the disease phenotype, reinforcing the idea that they represent excellent tools for understanding the role of lamin A/C in normal physiology and the clinical diversity associated with these diseases.
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Pharmacological inhibition of NF-κB prolongs lifespan of Drosophila melanogaster

Alexey Moskalev, Mikhail Shaposhnikov,

https://doi.org/10.18632/aging.100314 pp 391—394

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Moskalev A, Shaposhnikov M, . Pharmacological inhibition of NF-κB prolongs lifespan of Drosophila melanogaster. . 3:391-394. https://doi.org/10.18632/aging.100314

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Depletion of Ku70/80 reduces the levels of extrachromosomal telomeric circles and inhibits proliferation of ALT cells

Baomin Li, Sita Reddy, Lucio Comai,

https://doi.org/10.18632/aging.100308 pp 395—406

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Li B, Reddy S, Comai L, . Depletion of Ku70/80 reduces the levels of extrachromosomal telomeric circles and inhibits proliferation of ALT cells. . 3:395-406. https://doi.org/10.18632/aging.100308

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                TY  - JOUR
                AU  - Li, Baomin 
                AU  - Reddy, Sita 
                AU  - Comai, Lucio 
                TI  - Depletion of Ku70/80 reduces the levels of extrachromosomal telomeric circles and inhibits proliferation of ALT cells
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100308
                DO  - 10.18632/aging.100308
                SP  - 395
                EP  - 406
                PY  - 
                AB  - In normal cells, telomeres shorten each time a cell divides ultimately resulting in cell senescence. t In contrast, cancer cells counteract the loss of telomeric DNA either by inducing the expression of telomerase or by activating the Alternative Lengthening of Telomeres (ALT) pathway. ALT cells are characterized by heterogeneous telomeres and the presence of extrachromosomal circular double-stranded DNA molecules containing telomeric repeat sequences. These telomeric circles (t-circles) are thought to be generated through a recombination process and utilized as templates for telomere elongation by rolling-circle-replication, although their precise mechanism of formation and role in telomere maintenance and cell proliferation is largely unknown. Here we show that shRNA-mediated knockdown of the Ku70/80 heterodimer, a factor with functions at both pathological and natural DNA ends, inhibits ALT cell growth and results in a significant decrease in the levels of t-circles without affecting overall telomere length. These findings demonstrate that non homology-based processes contribute to the maintenance of t-circles and proliferation of ALT cells.
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Reversing the aging stromal phenotype prevents carcinoma initiation

Davina A. Lewis, Jeffrey B. Travers, Christiane Machado, Ally-Khan Somani, Dan F Spandau,

https://doi.org/10.18632/aging.100318 pp 407—416

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Lewis DA, Travers JB, Machado C, Somani A, Spandau DF, . Reversing the aging stromal phenotype prevents carcinoma initiation. . 3:407-416. https://doi.org/10.18632/aging.100318

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                TY  - JOUR
                AU  - Lewis, Davina A. 
                AU  - Travers, Jeffrey B. 
                AU  - Machado, Christiane 
                AU  - Somani, Ally-Khan 
                AU  - Spandau, Dan F 
                TI  - Reversing the aging stromal phenotype prevents carcinoma initiation
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100318
                DO  - 10.18632/aging.100318
                SP  - 407
                EP  - 416
                PY  - 
                AB  - The accumulation of senescent stromal cells in aging tissue changes the local microenvironment from normal to a state similar to chronic inflammation. This inflammatory microenvironment can stimulate the proliferation of epithelial cells containing DNA mutations which can ultimately lead to cancer. Using geriatric skin as a model, we demonstrated that senescent fibroblasts also alter how epithelial keratinocytes respond to genotoxic stress, due to the silencing of IGF-1 expression in geriatric fibroblasts. These data indicate that in addition to promoting epithelial tumor growth, senescent fibroblasts also can promote carcinogenic initiation. We hypothesized that commonly used therapeutic stromal wounding therapies can reduce the percentage of senescent fibroblasts and consequently prevent the formation of keratinocytes proliferating with DNA mutations following acute genotoxic (UVB) stress. Sun-protected skin on the lower back of geriatric human volunteers was wounded by dermabrasion and the skin was allowed to heal for three months. In geriatric skin, we found that dermabrasion wounding decreases the proportion of senescent fibroblasts found in geriatric dermis, increases the expression of IGF-1, and restores the appropriate UVB response to epidermal keratinocytes in geriatric skin. Therefore, dermal rejuvenation therapies may play a significant role in preventing the initiation of skin cancer in geriatric patients.
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Accelerated in vivo epidermal telomere loss in Werner syndrome

Naoshi Ishikawa, Ken-Ichi Nakamura, Naotaka Izumiyama-Shimomura, Junko Aida, Akio Ishii, Makoto Goto, Yuichi Ishikawa, Reimi Asaka, Masaaki Matsuura, Atsushi Hatamochi, Mie Kuroiwa, Kaiyo Takubo,

https://doi.org/10.18632/aging.100315 pp 417—429

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Ishikawa N, Nakamura K, Izumiyama-Shimomura N, Aida J, Ishii A, Goto M, Ishikawa Y, Asaka R, Matsuura M, Hatamochi A, Kuroiwa M, Takubo K, . Accelerated in vivo epidermal telomere loss in Werner syndrome. . 3:417-429. https://doi.org/10.18632/aging.100315

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                TY  - JOUR
                AU  - Ishikawa, Naoshi 
                AU  - Nakamura, Ken-Ichi 
                AU  - Izumiyama-Shimomura, Naotaka 
                AU  - Aida, Junko 
                AU  - Ishii, Akio 
                AU  - Goto, Makoto 
                AU  - Ishikawa, Yuichi 
                AU  - Asaka, Reimi 
                AU  - Matsuura, Masaaki 
                AU  - Hatamochi, Atsushi 
                AU  - Kuroiwa, Mie 
                AU  - Takubo, Kaiyo 
                TI  - Accelerated <i>in vivo</i> epidermal telomere loss in Werner syndrome
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100315
                DO  - 10.18632/aging.100315
                SP  - 417
                EP  - 429
                PY  - 
                AB  - Many data pertaining to the accelerated telomere loss in cultured cells derived from Werner syndrome (WS), a representative premature aging syndrome, have been accumulated. However, there have been no definitive data on in vivo telomere shortening in WS patients. In the present study, we measured terminal restriction fragment (TRF) lengths of 10 skin samples collected from extremities of 8 WS patients aged between 30 and 61 years that had been surgically amputated because of skin ulceration, and estimated the annual telomere loss. Whereas the values of TRF length in younger WS patients (in their thirties) were within the normal range, those in older WS patients were markedly shorter relative to non-WS controls. Regression analyses indicated that the TRF length in WS was significantly shorter than that in controls (p &lt; 0.001). Furthermore, we found that TRF lengths in muscle adjacent to the examined epidermis were also significantly shorter than those of controls (p = 0.047). These data demonstrate for the first time that in vivo telomere loss is accelerated in systemic organs of WS patients, suggesting that abnormal telomere erosion is one of the major causes of early onset of age-related symptoms and a predisposition to sarcoma and carcinoma in WS.
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The physiological roles of Sirt1 in skeletal muscle

Patricia S. Pardo, Aladin M. Boriek,

https://doi.org/10.18632/aging.100312 pp 430—437

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Pardo PS, Boriek AM, . The physiological roles of Sirt1 in skeletal muscle. . 3:430-437. https://doi.org/10.18632/aging.100312

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Reversing B cell aging

Ramit Mehr, Doron Melamed,

https://doi.org/10.18632/aging.100313 pp 438—443

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Mehr R, Melamed D, . Reversing B cell aging. . 3:438-443. https://doi.org/10.18632/aging.100313

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                TY  - JOUR
                AU  - Mehr, Ramit 
                AU  - Melamed, Doron 
                TI  - Reversing B cell aging
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100313
                DO  - 10.18632/aging.100313
                SP  - 438
                EP  - 443
                PY  - 
                AB  - Age-related alterations in the cellular composition of the B lineage are a major cause of the poor antibody response to vaccination and to infectious agents among the elderly population. The mechanisms leading to these changes are poorly understood. Recently, we have shown that these changes reflect, at least in part, homeostatic pressures imposed by long-lived B cells that accumulate with aging, and that aging in the B lineage can be reversed upon alteration of B cell homeostasis by depletion. Here we discuss homeostatic causes for B lineage immunosenescence, and the potential for its rejuvenation.
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Resveratrol-activated SIRT1 in liver and pancreatic β-cells: a Janus head looking to the same direction of metabolic homeostasis

Laurène Vetterli, Pierre Maechler,

https://doi.org/10.18632/aging.100304 pp 444—449

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Vetterli L, Maechler P, . Resveratrol-activated SIRT1 in liver and pancreatic β-cells: a Janus head looking to the same direction of metabolic homeostasis. . 3:444-449. https://doi.org/10.18632/aging.100304

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                TY  - JOUR
                AU  - Vetterli, Laurène 
                AU  - Maechler, Pierre 
                TI  - Resveratrol-activated SIRT1 in liver and pancreatic β-cells: a Janus head looking to the same direction of metabolic homeostasis
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100304
                DO  - 10.18632/aging.100304
                SP  - 444
                EP  - 449
                PY  - 
                AB  - Sirtuins are energy sensors which mediate effects of calorie restriction-induced lifespan extension. The mammalian sirtuin homolog SIRT1 is a protein deacetylase playing a central role in metabolic homeostasis. SIRT1 is one of the targets of resveratrol, a polyphenol that has been shown to increase lifespan and to protect animal models against high-calorie diet induced obesity and insulin resistance. The beneficial effects of resveratrol mediated by SIRT1 activation can be contributed by different organs. Among them, the liver and pancreatic β-cells have been shown to be responsive to resveratrol in a SIRT1-dependent manner. Downstream of SIRT1, transcription factors being activated are tissue-specific, in turn inducing expression of metabolic genes in an apparent paradoxical way. In this review, we discuss specificities of SIRT1 effects in the liver versus pancreatic β-cells, ultimately converging towards metabolic homeostasis at the organism level.
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Hyperactive when young, hypoactive and overweight when aged: Connecting the dots in the story about locomotor activity, body mass, and aging in Trpv1 knockout mice

Samuel P. Wanner, Andras Garami, Andrej A. Romanovsky,

https://doi.org/10.18632/aging.100306 pp 450—454

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Wanner SP, Garami A, Romanovsky AA, . Hyperactive when young, hypoactive and overweight when aged: Connecting the dots in the story about locomotor activity, body mass, and aging in Trpv1 knockout mice. . 3:450-454. https://doi.org/10.18632/aging.100306

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                TY  - JOUR
                AU  - Wanner, Samuel P. 
                AU  - Garami, Andras 
                AU  - Romanovsky, Andrej A. 
                TI  - Hyperactive when young, hypoactive and overweight when aged: Connecting the dots in the story about locomotor activity, body mass, and aging in <i>Trpv1</i> knockout mice
                JO  - 
                JA  - 
                VL  - 3
                IS  - 4
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100306
                DO  - 10.18632/aging.100306
                SP  - 450
                EP  - 454
                PY  - 
                AB  - We have recently found that, at a young age, transient receptor potential vanilloid-1 (Trpv1) knockout (−/−) mice have a higher locomotor activity than their wild-type littermates (+/+). We have also found that, with age, Trpv1−/− mice become substantially heavier than Trpv1+/+ controls, thus forming a paradoxical association between locomotor hyperactivity and overweight. The present study solves this contradiction. By using two experimental paradigms, we show that aged Trpv1−/− mice have not an increased, but a decreased, locomotor activity, as compared to age-matched Trpv1+/+ controls. We also confirm that aged Trpv1−/− mice are overweight. We conclude that TRPV1 channels are involved in the regulation of both general locomotor activity and body mass in an age-dependent manner.
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Volume 3, Issue 4

Commentaries

Barrie Peck, Almut Schulze,

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Robert M. Brosh Jr.,

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João Pedro de Magalhães,

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Silvestre Alavez, Gordon J. Lithgow,

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Mario G. Mirisola, Valter D. Longo,

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Christian Sell,

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Chen Zhao, Douglas Vollrath,

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Javier A. Menendez, Sílvia Cufí, Cristina Oliveras-Ferraros, Luciano Vellon, Jorge Joven, Alejandro Vazquez-Martin,

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Review

Yme U. van der Velden, Anna-Pavlina G. Haramis,

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Research Papers

Daria Zhebrun, Yulia Kudryashova, Alina Babenko, Alexei Maslyansky, Natalya Kunitskaya, Daria Popcova, Alexandra Klushina, Elena Grineva, Anna Kostareva, Evgeny Shlyakhto,

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Andreea Soare, Roberto Cangemi, Daniela Omodei, John O. Holloszy, Luigi Fontana,

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Jenny CY Ho, Ting Zhou, Wing-Hon Lai, Yinghua Huang, Yau-Chi Chan, Xingyan Li, Navy LY Wong, Yanhua Li, Ka-Wing Au, Dongsheng Guo, Jianyong Xu, Chung-Wah Siu, Duanqing Pei, Hung-Fat Tse, Miguel Angel Esteban,

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Alexey Moskalev, Mikhail Shaposhnikov,

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Baomin Li, Sita Reddy, Lucio Comai,

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Davina A. Lewis, Jeffrey B. Travers, Christiane Machado, Ally-Khan Somani, Dan F Spandau,

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Naoshi Ishikawa, Ken-Ichi Nakamura, Naotaka Izumiyama-Shimomura, Junko Aida, Akio Ishii, Makoto Goto, Yuichi Ishikawa, Reimi Asaka, Masaaki Matsuura, Atsushi Hatamochi, Mie Kuroiwa, Kaiyo Takubo,

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Research Perspectives

Patricia S. Pardo, Aladin M. Boriek,

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Ramit Mehr, Doron Melamed,

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Laurène Vetterli, Pierre Maechler,

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