Volume 7, Issue 6

Synergy between chemotherapy and cancer vaccination

Tetje C. van der Sluis, Sjoerd H. van der Burg, Cornelis J.M. Melief,

https://doi.org/10.18632/aging.100752 pp 340—341

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van der Sluis TC, van der Burg SH, Melief CJ, . Synergy between chemotherapy and cancer vaccination. . 7:340-341. https://doi.org/10.18632/aging.100752

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LK or IGF1R: When selectivity hurts

Igor Puzanov, Alexandra Hess,

https://doi.org/10.18632/aging.100753 pp 342—343

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Ras: structural details to guide direct targeting

Carla Mattos,

https://doi.org/10.18632/aging.100754 pp 344—345

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p38 MAPK in MDS

Irene Gañán‐Gómez, Zachary S. Bohannan, Guillermo Garcia‐Manero,

https://doi.org/10.18632/aging.100757 pp 346—347

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The usual SASPects of liver cancer

Amaia Lujambio, Augusto Villanueva,

https://doi.org/10.18632/aging.100758 pp 348—349

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Intratumor heterogeneity in HCC

Juliane Friemel, Lukas Frick, Achim Weber,

https://doi.org/10.18632/aging.100760 pp 350—351

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Low-dose radiation cancer susceptibility models

Jian-Hua Mao, Antoine M. Snijders,

https://doi.org/10.18632/aging.100767 pp 352—353

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Immunotherapy for acute leukemia

Michael Boyiadzis, Theresa L. Whiteside, Steven Z. Pavletic,

https://doi.org/10.18632/aging.100768 pp 354—355

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Pro‐tumorigenic role of ERα in prostate cancer cells

Luc Furic, Mitchell G. Lawrence, Gail P. Risbridger,

https://doi.org/10.18632/aging.100769 pp 356—357

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Immune infiltrate in cancer

Gautier Stoll, Laurence Zitvogel, Guido Kroemer,

https://doi.org/10.18632/aging.100770 pp 358—359

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Very long-term survival in pancreatic cancer

Marco Dal Molin, Laura D Wood,

https://doi.org/10.18632/aging.100771 pp 360—361

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Meeting Report: International Symposium on the Genetics of Aging and Life History II

Murat Artan, Ara B. Hwang, Seung‐Jae V. Lee, Hong Gil Nam,

https://doi.org/10.18632/aging.100762 pp 362—369

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Artan M, Hwang AB, Lee SV, Nam HG, . Meeting Report: International Symposium on the Genetics of Aging and Life History II. . 7:362-369. https://doi.org/10.18632/aging.100762

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                TY  - JOUR
                AU  - Artan, Murat 
                AU  - Hwang, Ara B. 
                AU  - Lee, Seung‐Jae V. 
                AU  - Nam, Hong Gil 
                TI  - Meeting Report: International Symposium on the Genetics of Aging and Life History II
                JO  - 
                JA  - 
                VL  - 7
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100762
                DO  - 10.18632/aging.100762
                SP  - 362
                EP  - 369
                PY  - 
                AB  - The second International Symposium on the Genetics of Aging and Life History was held at the campus of Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu, South Korea, from May 14 to 16, 2014. Many leading scientists in the field of aging research from all over the world contributed to the symposium by attending and presenting their recent work and thoughts. The aim of the symposium was to stimulate international collaborations and interactions among scientists who work on the biology of aging. In the symposium, the most recent and exciting work on aging research was presented, covering a wide range of topics, including the genetics of aging, age‐associated diseases, and cellular senescence. The work was conducted in various organisms, including C. elegans, mice, plants, and humans. Topics covered in the symposium stimulated discussion of novel directions for future research on aging. The meeting ended with a commitment for the third International Symposium on the Genetics of Aging and Life History, which will be held in 2016.
                ER  -

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Interstitial pericytes decrease in aged mouse kidneys

Ania Stefanska, Diana Eng, Natalya Kaverina, Jeremy S. Duffield, Jeffrey W. Pippin, Peter Rabinovitch, Stuart J. Shankland,

https://doi.org/10.18632/aging.100756 pp 370—382

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Stefanska A, Eng D, Kaverina N, Duffield JS, Pippin JW, Rabinovitch P, Shankland SJ, . Interstitial pericytes decrease in aged mouse kidneys. . 7:370-382. https://doi.org/10.18632/aging.100756

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                TY  - JOUR
                AU  - Stefanska, Ania 
                AU  - Eng, Diana 
                AU  - Kaverina, Natalya 
                AU  - Duffield, Jeremy S. 
                AU  - Pippin, Jeffrey W. 
                AU  - Rabinovitch, Peter 
                AU  - Shankland, Stuart J. 
                TI  - Interstitial pericytes decrease in aged mouse kidneys
                JO  - 
                JA  - 
                VL  - 7
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100756
                DO  - 10.18632/aging.100756
                SP  - 370
                EP  - 382
                PY  - 
                AB  - With increasing age, the kidney undergoes characteristic changes in the glomerular and tubulo-interstitial compartments, which are ultimately accompanied by reduced kidney function. Studies have shown age-related loss of peritubular vessels. Normal peritubular vessel tone, function and survival depend on neighboring pericytes. Pericyte detachment leads to vascular damage, which can be accompanied by their differentiation to fibroblasts and myofibroblasts, a state that favors matrix production. To better understand the fate of pericytes in the aged kidney, 27 month-old mice were studied. Compared to 3 month-old young adult mice, aged kidneys showed a substantial decrease in capillaries, identified by CD31 staining, in both cortex and medulla. This was accompanied by a marked decrease in surrounding NG2+/PDGFRß+ pericytes. This decrease was more pronounced in the medulla. Capillaries devoid of pericytes were typically dilated in aged mice. Aged kidneys were also characterized by interstitial fibrosis due to increased collagen-I and -III staining. This was accompanied by an increase in the number of pericytes that acquired a pro-fibrotic phenotype, identified by increased PDGFRß+/αSMA+ staining. These findings are consistent with the decline in kidney interstitial pericytes as a critical step in the development of changes to the peritubular vasculature with aging, and accompanying fibrosis.
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High-glucose diets have sex-specific effects on aging in C. elegans: toxic to hermaphrodites but beneficial to males

Marjorie R. Liggett, Michael J. Hoy, Michae Mastroianni, Michelle A. Mondoux,

https://doi.org/10.18632/aging.100759 pp 383—388

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Liggett MR, Hoy MJ, Mastroianni M, Mondoux MA, . High-glucose diets have sex-specific effects on aging in C. elegans: toxic to hermaphrodites but beneficial to males. . 7:383-388. https://doi.org/10.18632/aging.100759

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Provider: 
 TY - JOUR
 AU - Liggett, Marjorie R. 
 AU - Hoy, Michael J. 
 AU - Mastroianni, Michae 
 AU - Mondoux, Michelle A. 
 TI - High-glucose diets have sex-specific effects on aging in C. elegans: toxic to hermaphrodites but beneficial to males
 JO - 
 JA - 
 VL - 7
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.100759
 DO - 10.18632/aging.100759
 SP - 383
 EP - 388
 PY - 
 AB - Diet and sex are important determinants of lifespan. In humans, high sugar diets, obesity, and type 2 diabetes correlate with decreased lifespan, and females generally live longer than males. The nematode Caenorhabditis elegans is a classical model for aging studies, and has also proven useful for characterizing the response to high‐glucose diets. However, studies on male animals are lacking. We found a surprising dichotomy: glucose regulates lifespan and aging in a sex‐specific manner, with beneficial effects on males compared to toxic effects on hermaphrodites. High‐glucose diet resulted in greater mobility with age for males, along with a modest increase in median lifespan. In contrast, high‐glucose diets decrease both lifespan and mobility for hermaphrodites. Understanding sex‐specific responses to high‐glucose diets will be important for determining which evolutionarily conserved glucose‐responsive pathways that regulate aging are “universal” and which are likely to be cell‐type or sex‐specific.
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Transcriptome and ultrastructural changes in dystrophic Epidermolysis bullosa resemble skin aging

Jenny S. Breitenbach, Mark Rinnerthaler, Andrea Trost, Manuela Weber, Alfred Klausegger, Christina Gruber, Daniela Bruckner, Herbert A. Reitsamer, Johann W. Bauer, Michael Breitenbach,

https://doi.org/10.18632/aging.100755 pp 389—411

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Breitenbach JS, Rinnerthaler M, Trost A, Weber M, Klausegger A, Gruber C, Bruckner D, Reitsamer HA, Bauer JW, Breitenbach M, . Transcriptome and ultrastructural changes in dystrophic Epidermolysis bullosa resemble skin aging. . 7:389-411. https://doi.org/10.18632/aging.100755

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                TY  - JOUR
                AU  - Breitenbach, Jenny S. 
                AU  - Rinnerthaler, Mark 
                AU  - Trost, Andrea 
                AU  - Weber, Manuela 
                AU  - Klausegger, Alfred 
                AU  - Gruber, Christina 
                AU  - Bruckner, Daniela 
                AU  - Reitsamer, Herbert A. 
                AU  - Bauer, Johann W. 
                AU  - Breitenbach, Michael 
                TI  - Transcriptome and ultrastructural changes in dystrophic Epidermolysis bullosa resemble skin aging
                JO  - 
                JA  - 
                VL  - 7
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100755
                DO  - 10.18632/aging.100755
                SP  - 389
                EP  - 411
                PY  - 
                AB  - The aging process of skin has been investigated recently with respect to mitochondrial function and oxidative stress. We have here observed striking phenotypic and clinical similarity between skin aging and recessive dystrophic Epidermolysis bullosa (RDEB), which is caused by recessive mutations in the gene coding for collagen VII, COL7A1. Ultrastructural changes, defects in wound healing, and inflammation markers are in part shared with aged skin. We have here compared the skin transcriptomes of young adults suffering from RDEB with that of sex‐ and age‐matched healthy probands. In parallel we have compared the skin transcriptome of healthy young adults with that of elderly healthy donors. Quite surprisingly, there was a large overlap of the two gene lists that concerned a limited number of functional protein families. Most prominent among the proteins found are a number of proteins of the cornified envelope or proteins mechanistically involved in cornification and other skin proteins. Further, the overlap list contains a large number of genes with a known role in inflammation. We are documenting some of the most prominent ultrastructural and protein changes by immunofluorescence analysis of skin sections from patients, old individuals, and healthy controls.
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The influence of gender on inheritance of exceptional longevity

Jennifer A. Deluty, Gil Atzmon, Jill Crandall, Nir Barzilai, Sofiya Milman,

https://doi.org/10.18632/aging.100763 pp 412—418

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Deluty JA, Atzmon G, Crandall J, Barzilai N, Milman S, . The influence of gender on inheritance of exceptional longevity. . 7:412-418. https://doi.org/10.18632/aging.100763

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                TY  - JOUR
                AU  - Deluty, Jennifer A. 
                AU  - Atzmon, Gil 
                AU  - Crandall, Jill 
                AU  - Barzilai, Nir 
                AU  - Milman, Sofiya 
                TI  - The influence of gender on inheritance of exceptional longevity
                JO  - 
                JA  - 
                VL  - 7
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100763
                DO  - 10.18632/aging.100763
                SP  - 412
                EP  - 418
                PY  - 
                AB  - While the search for genetic contributors to exceptional longevity has yielded candidates, gender differences in inheritance have generally not been considered. The aim of this study was to investigate gender specific differences in the inheritance of exceptional longevity. Using a standardized questionnaire, we assessed the parental ages of death of Ashkenazi Jews with exceptional longevity and their spouses without exceptional longevity, who served as controls (n=1,114). Mothers of centenarian males and females had significantly longer lifespans compared to the mothers of non‐ centenarians, 79.0 ± 13.4 vs. 73.0 ± 16.3 years, p&lt;0.01 and 75.7 ± 15.8 vs. 70.5 ± 18.0 years, p=0.02, respectively. There was also a trend toward longer lifespan among the fathers of centenarian men compared to the lifespan of fathers of non‐ centenarian men, 73.5 ± 17.0 vs. 69.5 ±15.0 years, p=0.07. The lifespan did not differ between the fathers of centenarian and non‐centenarian daughters. Logistic regression models revealed that the odds of being a centenarian for the female and male offspring increased by 21% and 31%, respectively, for every additional 10 years of life achieved by the mother (p&lt;0.05). These findings support a gender‐specific inheritance pattern of human longevity and may help focus the search for longevity genes.
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Tissue-specific autophagy responses to aging and stress in C. elegans

Hannah C. Chapin, Megan Okada, Alexey J. Merz, Dana L. Miller,

https://doi.org/10.18632/aging.100765 pp 419—434

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Chapin HC, Okada M, Merz AJ, Miller DL, . Tissue-specific autophagy responses to aging and stress in C. elegans. . 7:419-434. https://doi.org/10.18632/aging.100765

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 TY - JOUR
 AU - Chapin, Hannah C. 
 AU - Okada, Megan 
 AU - Merz, Alexey J. 
 AU - Miller, Dana L. 
 TI - Tissue-specific autophagy responses to aging and stress in C. elegans
 JO - 
 JA - 
 VL - 7
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.100765
 DO - 10.18632/aging.100765
 SP - 419
 EP - 434
 PY - 
 AB - Cellular function relies on a balance between protein synthesis and breakdown. Macromolecular breakdown through autophagy is broadly required for cellular and tissue development, function, and recovery from stress. While Caenorhabditis elegans is frequently used to explore cellular responses to development and stress, the most common assays for autophagy in this system lack tissue-level resolution. Different tissues within an organism have unique functional characteristics and likely vary in their reliance on autophagy under different conditions. To generate a tissue-specific map of autophagy in C. elegans we used a dual fluorescent protein (dFP) tag that releases monomeric fluorescent protein (mFP) upon arrival at the lysosome. Tissue-specific expression of dFP::LGG-1 revealed autophagic flux in all tissues, but mFP accumulation was most dramatic in the intestine. We also observed variable responses to stress: starvation increased autophagic mFP release in all tissues, whereas anoxia primarily increased intestinal autophagic flux. We observed autophagic flux with tagged LGG-1, LGG-2, and two autophagic cargo reporters: a soluble cytoplasmic protein, and mitochondrial TOMM-7. Finally, an increase in mFP in older worms was consistent with an age-dependent shift in proteostasis. These novel measures of autophagic flux in C. elegans reveal heterogeneity in autophagic response across tissues during stress and aging.
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Premature aging of the hippocampal neurogenic niche in adult Bmal1‐ deficient mice

Amira A. H. Ali, Beryl Schwarz‐Herzke, Anna Stahr, Timour Prozorovski, Orhan Aktas, Charlotte von Gall,

https://doi.org/10.18632/aging.100764 pp 435—449

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Ali AAH, Schwarz‐Herzke B, Stahr A, Prozorovski T, Aktas O, von Gall C, . Premature aging of the hippocampal neurogenic niche in adult Bmal1‐ deficient mice. . 7:435-449. https://doi.org/10.18632/aging.100764

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 TY - JOUR
 AU - Ali, Amira A. H. 
 AU - Schwarz‐Herzke, Beryl 
 AU - Stahr, Anna 
 AU - Prozorovski, Timour 
 AU - Aktas, Orhan 
 AU - von Gall, Charlotte 
 TI - Premature aging of the hippocampal neurogenic niche in adult Bmal1‐ deficient mice
 JO - 
 JA - 
 VL - 7
 IS - 6
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.100764
 DO - 10.18632/aging.100764
 SP - 435
 EP - 449
 PY - 
 AB - Hippocampal neurogenesis undergoes dramatic age‐related changes. Mice with targeted deletion of the clock gene Bmal1 (Bmal1‐/‐) show disrupted regulation of reactive oxygen species homeostasis, accelerated aging, neurodegeneration and cognitive deficits. As proliferation of neuronal progenitor/precursor cells (NPCs) is enhanced in young Bmal1‐/‐ mice, we tested the hypothesis that this results in premature aging of hippocampal neurogenic niche in adult Bmal1‐/‐ mice as compared to wildtype littermates. We found significantly reduced pool of hippocampal NPCs, scattered distribution, enhanced survival of NPCs and an increased differentiation of NPCs into the astroglial lineage at the expense of the neuronal lineage. Immunoreaction of the redox sensitive histone deacetylase Sirtuine 1, peroxisomal membrane protein at 70kDa and expression of the cell cycle inhibitor p21 Waf1/CIP1 were increased in adult Bmal1‐/‐ mice. In conclusion, genetic disruption of the molecular clockwork leads to accelerated age‐dependent decline in adult neurogenesis presumably as a consequence of oxidative stress.
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Erratum: Burden of disease variants in participants of the long life family study

Meredith Stevenson, Harold Bae, Nicole Schupf, Stacy Andersen, Qunyuan Zhang, Thomas Perls, Paola Sebastiani,

https://doi.org/10.18632/aging.100761 pp 450

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Stevenson M, Bae H, Schupf N, Andersen S, Zhang Q, Perls T, Sebastiani P, . Erratum: Burden of disease variants in participants of the long life family study. . 7:450-450. https://doi.org/10.18632/aging.100761

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Volume 7, Issue 6

Editorials

Tetje C. van der Sluis, Sjoerd H. van der Burg, Cornelis J.M. Melief,

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Igor Puzanov, Alexandra Hess,

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Carla Mattos,

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Irene Gañán‐Gómez, Zachary S. Bohannan, Guillermo Garcia‐Manero,

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Amaia Lujambio, Augusto Villanueva,

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Juliane Friemel, Lukas Frick, Achim Weber,

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Jian-Hua Mao, Antoine M. Snijders,

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Michael Boyiadzis, Theresa L. Whiteside, Steven Z. Pavletic,

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Luc Furic, Mitchell G. Lawrence, Gail P. Risbridger,

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Gautier Stoll, Laurence Zitvogel, Guido Kroemer,

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Marco Dal Molin, Laura D Wood,

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Meeting Report

Murat Artan, Ara B. Hwang, Seung‐Jae V. Lee, Hong Gil Nam,

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Research Papers

Ania Stefanska, Diana Eng, Natalya Kaverina, Jeremy S. Duffield, Jeffrey W. Pippin, Peter Rabinovitch, Stuart J. Shankland,

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Marjorie R. Liggett, Michael J. Hoy, Michae Mastroianni, Michelle A. Mondoux,

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Jenny S. Breitenbach, Mark Rinnerthaler, Andrea Trost, Manuela Weber, Alfred Klausegger, Christina Gruber, Daniela Bruckner, Herbert A. Reitsamer, Johann W. Bauer, Michael Breitenbach,

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Jennifer A. Deluty, Gil Atzmon, Jill Crandall, Nir Barzilai, Sofiya Milman,

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Hannah C. Chapin, Megan Okada, Alexey J. Merz, Dana L. Miller,

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Amira A. H. Ali, Beryl Schwarz‐Herzke, Anna Stahr, Timour Prozorovski, Orhan Aktas, Charlotte von Gall,

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Erratum

Meredith Stevenson, Harold Bae, Nicole Schupf, Stacy Andersen, Qunyuan Zhang, Thomas Perls, Paola Sebastiani,

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