Volume 3, Issue 7

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Srikantan S, Gorospe M, . Altered glycobiology of stem cells linked to age-related osteoarthritis. . 3:663-664. https://doi.org/10.18632/aging.100356

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Provider: TY - JOUR AU - Srikantan, Subramanya AU - Gorospe, Myriam TI - Altered glycobiology of stem cells linked to age-related osteoarthritis JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100356 DO - 10.18632/aging.100356 SP - 663 EP - 664 PY - ER -

Provider: TY - JOUR AU - Srikantan, Subramanya AU - Gorospe, Myriam TI - Altered glycobiology of stem cells linked to age-related osteoarthritis JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100356 DO - 10.18632/aging.100356 SP - 663 EP - 664 PY - AB - ER -

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Rizzo M, Evangelista M, Simili M, Mariani L, Pitto L, Rainaldi G, . Immortalization of MEF is characterized by the deregulation of specific miRNAs with potential tumor suppressor activity. . 3:665-671. https://doi.org/10.18632/aging.100353

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Provider: TY - JOUR AU - Rizzo, Milena AU - Evangelista, Monica AU - Simili, Marcella AU - Mariani, Laura AU - Pitto, Letizia AU - Rainaldi, Giuseppe TI - Immortalization of MEF is characterized by the deregulation of specific miRNAs with potential tumor suppressor activity JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100353 DO - 10.18632/aging.100353 SP - 665 EP - 671 PY - ER -

Provider: TY - JOUR AU - Rizzo, Milena AU - Evangelista, Monica AU - Simili, Marcella AU - Mariani, Laura AU - Pitto, Letizia AU - Rainaldi, Giuseppe TI - Immortalization of MEF is characterized by the deregulation of specific miRNAs with potential tumor suppressor activity JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100353 DO - 10.18632/aging.100353 SP - 665 EP - 671 PY - AB - The life span (Hayflick limit) of primary mouse embryo fibroblasts (MEF) in culture is variable but it is still unclear if the escape of the Hayflick limit is also variable. To address this point MEF were expanded every fifteen days (6T15) instead of every three days (6T3) until they became immortal. With this protocol MEF lifespan was extended and immortalization accordingly delayed. By testing a panel of genes (p19ARF, p16, p21) and miRNAs (miR-20a, miR-21, miR-28, miR-290) related to primary MEF senescence, a switch of p21 from up to down regulation, the down regulation of specific miRNAs as well as a massive shift from diploidy to hyperdiploidy were observed in coincidence with the resumption of cell proliferation. Collectively, these data indicate that the inactivation of genes and miRNAs, important in controlling cell proliferation, might be determinant for the escape from the Hayflick limit. In support of this hypothesis was the finding that some of the down regulated miRNAs transfected in immortalized MEF inhibited cell proliferation thus displaying a tumor suppressor-like activity. ER -

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Jiang SS, Chen C, Tseng K, Tsai F, Wang MJ, Chang I, Lin J, Lin S, . Gene expression profiling suggests a pathological role of human bone marrow-derived mesenchymal stem cells in aging-related skeletal diseases. . 3:672-684. https://doi.org/10.18632/aging.100355

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Provider: TY - JOUR AU - Jiang, Shih Sheng AU - Chen, Chung-Hsing AU - Tseng, Kuo-Yun AU - Tsai, Fang-Yu AU - Wang, Ming Jen AU - Chang, I-Shou AU - Lin, Jiunn-Liang AU - Lin, Shankung TI - Gene expression profiling suggests a pathological role of human bone marrow-derived mesenchymal stem cells in aging-related skeletal diseases JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100355 DO - 10.18632/aging.100355 SP - 672 EP - 684 PY - ER -

Provider: TY - JOUR AU - Jiang, Shih Sheng AU - Chen, Chung-Hsing AU - Tseng, Kuo-Yun AU - Tsai, Fang-Yu AU - Wang, Ming Jen AU - Chang, I-Shou AU - Lin, Jiunn-Liang AU - Lin, Shankung TI - Gene expression profiling suggests a pathological role of human bone marrow-derived mesenchymal stem cells in aging-related skeletal diseases JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100355 DO - 10.18632/aging.100355 SP - 672 EP - 684 PY - AB - Aging is associated with bone loss and degenerative joint diseases, in which the aging of bone marrow-derived mesenchymal stem cell (bmMSC) may play an important role. In this study, we analyzed the gene expression profiles of bmMSC from 14 donors between 36 and 74 years old, and obtained age-associated genes (in the background of osteoarthritis) and osteoarthritis-associated genes (in the background of old age). Pathway analysis of these genes suggests that alterations in glycobiology might play an important role in the aging of human bmMSC. On the other hand, antigen presentation and signaling of immune cells were the top pathways enriched by osteoarthritis-associated genes, suggesting that alteration in immunology of bmMSC might be involved in the pathogenesis of osteoarthritis. Most intriguingly, we found significant age-associated differential expression of HEXA, HEXB, CTSK, SULF1, ADAMTS5, SPP1, COL8A2, GPNMB, TNFAIP6, and RPL29; those genes have been implicated in the bone loss and the pathology of osteoporosis and osteoarthritis in aging. Collectively, our results suggest a pathological role of bmMSC in aging-related skeletal diseases, and suggest the possibility that alteration in the immunology of bmMSC might also play an important role in the etiology of adult-onset osteoarthritis. ER -

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Blagosklonny MV, . Progeria, rapamycin and normal aging: recent breakthrough. . 3:685-691. https://doi.org/10.18632/aging.100352

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Provider: TY - JOUR AU - Blagosklonny, Mikhail V. TI - Progeria, rapamycin and normal aging: recent breakthrough JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100352 DO - 10.18632/aging.100352 SP - 685 EP - 691 PY - ER -

Provider: TY - JOUR AU - Blagosklonny, Mikhail V. TI - Progeria, rapamycin and normal aging: recent breakthrough JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100352 DO - 10.18632/aging.100352 SP - 685 EP - 691 PY - AB - A recent discovery that rapamycin suppresses a pro-senescent phenotype in progeric cells not only suggests a non-toxic therapy for progeria but also implies its similarity with normal aging. For one, rapamycin is also known to suppress aging of regular human cells. Here I discuss four potential scenarios, comparing progeria with both normal and accelerated aging. This reveals further indications of rapamycin both for accelerated aging in obese and for progeria. ER -

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Ratajczak MZ, Kucia M, Liu R, Shin D, Bryndza E, Masternak MM, Tarnowski M, Ratajczak J, Bartke A, . RasGrf1: genomic imprinting, VSELs, and aging. . 3:692-697. https://doi.org/10.18632/aging.100354

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Provider: TY - JOUR AU - Ratajczak, Mariusz Z. AU - Kucia, Magda AU - Liu, Rui AU - Shin, Dong-Myung AU - Bryndza, Ewa AU - Masternak, Michal M. AU - Tarnowski, Maciej AU - Ratajczak, Janina AU - Bartke, Andrzej TI - RasGrf1: genomic imprinting, VSELs, and aging JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100354 DO - 10.18632/aging.100354 SP - 692 EP - 697 PY - ER -

Provider: TY - JOUR AU - Ratajczak, Mariusz Z. AU - Kucia, Magda AU - Liu, Rui AU - Shin, Dong-Myung AU - Bryndza, Ewa AU - Masternak, Michal M. AU - Tarnowski, Maciej AU - Ratajczak, Janina AU - Bartke, Andrzej TI - RasGrf1: genomic imprinting, VSELs, and aging JO - JA - VL - 3 IS - 7 PB - SN - UR - https://doi.org/10.18632/aging.100354 DO - 10.18632/aging.100354 SP - 692 EP - 697 PY - AB - Increase in life span in RasGrf1-deficient mice revealed that RasGrf1 deficiency promotes longevity. Interestingly, RasGrf1 is one of parentally imprinted genes transcribed from paternally-derived chromosome. Erasure of its imprinting results in RasGrf1 downregulation and has been demonstrated in a population of pluripotent adult tissues-derived very small embryonic like stem cells (VSELs), stem cells involved in tissue organ rejuvenation. Furthermore, based on recent observation that RasGrf1 signaling molecule is located downstream from insulin (Ins) and insulin like growth factor-1 (Igf-1) receptors, the extended life-span of RasGrf1−/− mice may support beneficial effect of reduced Ins/Igf-1 signaling on longevity. Similarly, downregulation of RasGrf1 in VSELs renders them resistant to chronic Ins/Igf-1 signaling and protects from premature depletion from adult tissues. Thus, the studies in RasGrf1−/− mice indicate that some of the imprinted genes may play a role in ontogenetic longevity and suggest that there are sex differences in life span that originate at the genome level. All this in toto supports a concept that the sperm genome may have a detrimental effect on longevity in mammals. We will discuss a role of RasGrf1 on life span in context of genomic imprinting and VSELs. ER -

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