HRasV12诱导小鼠骨骼肌母细胞凋亡,而非细胞衰老

IF 5.3 3区 医学 Q2 CELL BIOLOGY
Shinichiro Suzuki , Takuya Fukunaga , Tatsuya Hayashi , Tatsuro Egawa
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引用次数: 0

摘要

衰老是骨骼肌减少症的关键危险因素,骨骼肌减少症是一种影响骨骼肌的进行性疾病。衰老的一个标志是细胞衰老。为了研究小鼠成骨肌细胞的细胞衰老,我们尝试用HRasV12诱导细胞衰老。出乎意料的是,HRasV12没有诱导p16和p21等衰老标志物的表达,也没有在成肌细胞中观察到SA-β-gal阳性细胞。相反,HRasV12升高了成肌细胞中凋亡标志物的水平,如cleaved caspase-3、cleaved caspase-8和Bax与Bcl-2的比值。这些发现表明,HRasV12不会诱导小鼠骨骼肌成细胞衰老,但会引发细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
HRasV12 induces apoptosis, not cellular senescence in mouse skeletal myoblasts
Aging is a key risk factor for sarcopenia, a progressive disorder affecting skeletal muscle. One hallmark of aging is cellular senescence. To investigate cellular senescence in mouse skeletal myoblasts, we attempted to induce cellular senescence by HRasV12. Unexpectedly, HRasV12 did not induce the expression of senescence markers such as p16 and p21, and no SA-β-gal-positive cells were observed in the myoblasts. Instead, HRasV12 elevated the levels of apoptotic markers such as cleaved caspase-3, cleaved caspase-8, and the ratio of Bax to Bcl-2 in the myoblasts. These findings suggested that HRasV12 does not induce senescence, but triggers apoptotic cell death in mouse skeletal myoblasts.
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来源期刊
CiteScore
11.10
自引率
1.90%
发文量
79
审稿时长
32 days
期刊介绍: Mechanisms of Ageing and Development is a multidisciplinary journal aimed at revealing the molecular, biochemical and biological mechanisms that underlie the processes of aging and development in various species as well as of age-associated diseases. Emphasis is placed on investigations that delineate the contribution of macromolecular damage and cytotoxicity, genetic programs, epigenetics and genetic instability, mitochondrial function, alterations of metabolism and innovative anti-aging approaches. For all of the mentioned studies it is necessary to address the underlying mechanisms. Mechanisms of Ageing and Development publishes original research, review and mini-review articles. The journal also publishes Special Issues that focus on emerging research areas. Special issues may include all types of articles following peered review. Proposals should be sent directly to the Editor-in-Chief.
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