Volume 7, Issue 7

Ghosh P, . Heterotrimeric G proteins as emerging targets for network based therapy in cancer: End of a long futile campaign striking heads of a Hydra. . 7:469-474. https://doi.org/10.18632/aging.100781

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                TY  - JOUR
                AU  - Ghosh, Pradipta 
                TI  - Heterotrimeric G proteins as emerging targets for network based therapy in cancer: <i>End of a long futile campaign striking heads of a Hydra</i>
                JO  - 
                JA  - 
                VL  - 7
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100781
                DO  - 10.18632/aging.100781
                SP  - 469
                EP  - 474
                PY  - 
                AB  - Most common diseases, e.g., cancer are driven by not one, but multiple cell surface receptors that trigger and sustain a pathologic signaling network. The largest fraction of therapeutic agents that target individual receptors/pathways eventually fail due to the emergence of compensatory mechanisms that reestablish the pathologic network. Recently, a rapidly emerging paradigm has revealed GIV/Girdin as a central platform for receptor cross-talk which integrates signals downstream of a myriad of cell surface receptors, and modulates several key pathways within downstream signaling network, all via non-canonical activation of trimeric G proteins. Unlike canonical signal transduction via G proteins, which is spatially and temporally restricted, the temporal and spatial features of non-canonical activation of G protein via GIV is unusually unrestricted. Consequently, the GIV●G protein interface serves as a central hub allowing for control over several pathways within the pathologic signaling network, all at once. The relevance of this new paradigm in cancer and other disease states and the pros and cons of targeting the GIV●G protein interface are discussed
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Mitochondria-targeted antioxidant SkQ1 improves impaired dermal wound healing in old mice

Ilya A. Demyanenko, Ekaterina N. Popova, Vlada V. Zakharova, Olga P. Ilyinskaya, Tamara V. Vasilieva, Valeria P. Romashchenko, Artem V. Fedorov, Vasily N. Manskikh, Maxim V. Skulachev, Roman A. Zinovkin, Olga Yu. Pletjushkina, Vladimir P. Skulachev, Boris V. Chernyak,

https://doi.org/10.18632/aging.100772 pp 475—485

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Demyanenko IA, Popova EN, Zakharova VV, Ilyinskaya OP, Vasilieva TV, Romashchenko VP, Fedorov AV, Manskikh VN, Skulachev MV, Zinovkin RA, Pletjushkina OY, Skulachev VP, Chernyak BV, . Mitochondria-targeted antioxidant SkQ1 improves impaired dermal wound healing in old mice. . 7:475-485. https://doi.org/10.18632/aging.100772

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                TY  - JOUR
                AU  - Demyanenko, Ilya A. 
                AU  - Popova, Ekaterina N. 
                AU  - Zakharova, Vlada V. 
                AU  - Ilyinskaya, Olga P. 
                AU  - Vasilieva, Tamara V. 
                AU  - Romashchenko, Valeria P. 
                AU  - Fedorov, Artem V. 
                AU  - Manskikh, Vasily N. 
                AU  - Skulachev, Maxim V. 
                AU  - Zinovkin, Roman A. 
                AU  - Pletjushkina, Olga Yu. 
                AU  - Skulachev, Vladimir P. 
                AU  - Chernyak, Boris V. 
                TI  - Mitochondria-targeted antioxidant SkQ1 improves impaired dermal wound healing in old mice
                JO  - 
                JA  - 
                VL  - 7
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100772
                DO  - 10.18632/aging.100772
                SP  - 475
                EP  - 485
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Demyanenko, Ilya A. 
                AU  - Popova, Ekaterina N. 
                AU  - Zakharova, Vlada V. 
                AU  - Ilyinskaya, Olga P. 
                AU  - Vasilieva, Tamara V. 
                AU  - Romashchenko, Valeria P. 
                AU  - Fedorov, Artem V. 
                AU  - Manskikh, Vasily N. 
                AU  - Skulachev, Maxim V. 
                AU  - Zinovkin, Roman A. 
                AU  - Pletjushkina, Olga Yu. 
                AU  - Skulachev, Vladimir P. 
                AU  - Chernyak, Boris V. 
                TI  - Mitochondria-targeted antioxidant SkQ1 improves impaired dermal wound healing in old mice
                JO  - 
                JA  - 
                VL  - 7
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100772
                DO  - 10.18632/aging.100772
                SP  - 475
                EP  - 485
                PY  - 
                AB  - The process of skin wound healing is delayed or impaired in aging animals. To investigate the possible role of mitochondrial reactive oxygen species (mtROS) in cutaneous wound healing of aged mice, we have applied the mitochondria-targeted antioxidant SkQ1. The SkQ1 treatment resulted in accelerated resolution of the inflammatory phase, formation of granulation tissue, vascularization and epithelization of the wounds. The wounds of SkQ1-treated mice contained increased amount of myofibroblasts which produce extracellular matrix proteins and growth factors mediating granulation tissue formation. This effect resembled SkQ1-induced differentiation of fibroblasts to myofibroblast, observed earlier in vitro. The Transforming Growth Factor beta (TGFβ)produced by SkQ1-treated fibroblasts was found to stimulated motility of endothelial cells in vitro, an effect which may underlie pro-angiogenic action of SkQ1 in the wounds. In vitro experiments showed that SkQ1 prevented decomposition of VE-cadherin containing contacts and following increase in permeability of endothelial cells monolayer, induced by pro-inflammatory cytokine TNF. Prevention of excessive reaction of endothelium to the pro-inflammatory cytokine(s) might account for anti-inflammatory effect of SkQ1. Our findings point to an important role of mtROS in pathogenesis of age-related chronic wounds.
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Transgenic mice overexpressing glia maturation factor-β, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation

Rika Imai, Kanae Asai, Jun-ichi Hanai, Masaru Takenaka,

https://doi.org/10.18632/aging.100779 pp 486—499

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Imai R, Asai K, Hanai J, Takenaka M, . Transgenic mice overexpressing glia maturation factor-β, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation. . 7:486-499. https://doi.org/10.18632/aging.100779

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                TY  - JOUR
                AU  - Imai, Rika 
                AU  - Asai, Kanae 
                AU  - Hanai, Jun-ichi 
                AU  - Takenaka, Masaru 
                TI  - Transgenic mice overexpressing glia maturation factor-β, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation
                JO  - 
                JA  - 
                VL  - 7
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100779
                DO  - 10.18632/aging.100779
                SP  - 486
                EP  - 499
                PY  - 
                AB  - Glia Maturation Factor-β (GMF), a brain specific protein, is induced by proteinuria in renal tubules. Ectopic GMF overexpression causes apoptosis in vitro via cellular vulnerability to oxidative stress. In order to examine the roles of GMF in non-brain tissue, we constructed transgenic mice overexpressing GMF (GMF-TG). The GMF-TG mice exhibited appearance phenotypes associated with premature aging. The GMF-TG mice also demonstrated short lifespans and reduced hair regrowth, suggesting an accelerated aging process. The production of an abnormal lamin A, a nuclear envelope protein, plays a causal role in both normal aging and accelerated aging diseases, known as laminopathies. Importantly, we identified the abnormal lamin A (prelamin A), accompanied by a down-regulation of a lamin A processing enzyme (Zmpste24) in the kidney of the GMF-TG mice. The GMF-TG mice showed accelerated aging in the kidney, compared with wild-type mice, showing increased TGF-β1, CTGF gene and serum creatinine. The gene expression of p21/waf1 was increased at an earlier stage of life, at 10 weeks, which was in turn down-regulated at a later stage, at 60 weeks. In conclusion, we propose that GMF-TG mice might be a novel mouse model of accelerated aging, due to the abnormal lamin A.
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Removal of growth hormone receptor (GHR) in muscle of male mice replicates some of the health benefits seen in global GHR−/− mice

Edward O. List, Darlene E. Berryman, Yuji Ikeno, Gene B. Hubbard, Kevin Funk, Ross Comisford, Jonathan A. Young, Michael B. Stout, Tamar Tchkonia, Michal M. Masternak, Andrzej Bartke, James L. Kirkland, Richard A. Miller, John J. Kopchick,

https://doi.org/10.18632/aging.100766 pp 500—512

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List EO, Berryman DE, Ikeno Y, Hubbard GB, Funk K, Comisford R, Young JA, Stout MB, Tchkonia T, Masternak MM, Bartke A, Kirkland JL, Miller RA, et al, . Removal of growth hormone receptor (GHR) in muscle of male mice replicates some of the health benefits seen in global GHR−/− mice. . 7:500-512. https://doi.org/10.18632/aging.100766

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Provider: 
                TY  - JOUR
                AU  - List, Edward O. 
                AU  - Berryman, Darlene E. 
                AU  - Ikeno, Yuji 
                AU  - Hubbard, Gene B. 
                AU  - Funk, Kevin 
                AU  - Comisford, Ross 
                AU  - Young, Jonathan A. 
                AU  - Stout, Michael B. 
                AU  - Tchkonia, Tamar 
                AU  - Masternak, Michal M. 
                AU  - Bartke, Andrzej 
                AU  - Kirkland, James L. 
                AU  - Miller, Richard A. 
                AU  - Kopchick, John J. 
                TI  - Removal of growth hormone receptor (GHR) in muscle of male mice replicates some of the health benefits seen in global GHR−/− mice
                JO  - 
                JA  - 
                VL  - 7
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100766
                DO  - 10.18632/aging.100766
                SP  - 500
                EP  - 512
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - List, Edward O. 
                AU  - Berryman, Darlene E. 
                AU  - Ikeno, Yuji 
                AU  - Hubbard, Gene B. 
                AU  - Funk, Kevin 
                AU  - Comisford, Ross 
                AU  - Young, Jonathan A. 
                AU  - Stout, Michael B. 
                AU  - Tchkonia, Tamar 
                AU  - Masternak, Michal M. 
                AU  - Bartke, Andrzej 
                AU  - Kirkland, James L. 
                AU  - Miller, Richard A. 
                AU  - Kopchick, John J. 
                TI  - Removal of growth hormone receptor (GHR) in muscle of male mice replicates some of the health benefits seen in global GHR−/− mice
                JO  - 
                JA  - 
                VL  - 7
                IS  - 7
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100766
                DO  - 10.18632/aging.100766
                SP  - 500
                EP  - 512
                PY  - 
                AB  - Global disruption of the GH receptor in mice (GHR−/−) produces a large and reproducible extension in lifespan. Since lack of GH action in muscle resulting in improved glucose homeostasis is potentially a mechanism by which GHR−/− mice are long-lived, and since no information on muscle-specific GHR disruption in females is available, we generated and characterized a line of muscle-specific GHR disrupted (MuGHRKO) mice. As expected, male MuGHRKO mice had improved fasting blood glucose, insulin, c-peptide, and glucose tolerance. In contrast, female MuGHRKO mice exhibited normal glucose, insulin, and glucose tolerance. Body weight was mildly but significantly altered in opposite directions in males (decreased) and females (increased) compared to controls. Grip strength and treadmill endurance were unchanged with advanced age in both sexes, suggesting that the direct action of GH on muscle has minimal effect on age-related musculoskeletal frailty. Longevity was unchanged in both sexes at Ohio University and significantly increased for males at University of Michigan. These data suggest that removal of GHR in muscle of male MuGHRKO mice replicates some of the health benefits seen in global GHR−/− mice including improvements to glucose homeostasis and smaller body weight in males, which may explain the trends observed in lifespan.
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Volume 7, Issue 7

Editorials

Age cutoff in lymphoma diagnosis

Chi Y. Ok, Ken H. Young,

ATF5: development of oncogenic resistance to radiotherapy

Seiichiro Ishihara, Hisashi Haga,

Kinase independent oncogenic cyclin D1

Mathew C. Casimiro, Andrew Arnold, Richard G. Pestell,

Stem cells, aging and cancers

Arnold J. Levine,

A brave new MYC-amplified world

Marc S. Weinberg, Jonathan R. Hart, Peter K. Vogt,

CSN6-COP1 axis in cancer

Hyun Ho Choi, Mong-Hong Lee,

Stopping MYC in its tracks

Eduard Stefan, Jonathan R. Hart, Klaus Bister,

Hypoxia metabolism in ageing

Alessandro Valli, Adrian L Harris, Benedikt M Kessler,

β-catenin in epithelial tumorigenesis

Tsai-Ling Lu, Chun-Ming Chen,

Research Perspective

Heterotrimeric G proteins as emerging targets for network based therapy in cancer: End of a long futile campaign striking heads of a Hydra

Pradipta Ghosh,

Research Papers

Mitochondria-targeted antioxidant SkQ1 improves impaired dermal wound healing in old mice

Ilya A. Demyanenko, Ekaterina N. Popova, Vlada V. Zakharova, Olga P. Ilyinskaya, Tamara V. Vasilieva, Valeria P. Romashchenko, Artem V. Fedorov, Vasily N. Manskikh, Maxim V. Skulachev, Roman A. Zinovkin, Olga Yu. Pletjushkina, Vladimir P. Skulachev, Boris V. Chernyak,

Transgenic mice overexpressing glia maturation factor-β, an oxidative stress inducible gene, show premature aging due to Zmpste24 down-regulation

Rika Imai, Kanae Asai, Jun-ichi Hanai, Masaru Takenaka,

Removal of growth hormone receptor (GHR) in muscle of male mice replicates some of the health benefits seen in global GHR−/− mice

Edward O. List, Darlene E. Berryman, Yuji Ikeno, Gene B. Hubbard, Kevin Funk, Ross Comisford, Jonathan A. Young, Michael B. Stout, Tamar Tchkonia, Michal M. Masternak, Andrzej Bartke, James L. Kirkland, Richard A. Miller, John J. Kopchick,

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