A novel role of Fas in delaying cellular senescence.

A novel role of Fas in delaying cellular senescence.
复制标题

DOI:
10.1016/j.heliyon.2023.e13451
复制
发表时间:
2023-03
期刊:
影响因子:
4
通讯作者:
Huang, Gonghua
Huang, Gonghua
中科院分区:
综合性期刊4区
文献类型:
--
作者:
Saha, Chaitrali;Li, Jingyu;Sun, Xuerong;Liu, Xinguang;Huang, Gonghua

文献摘要

参考文献

相似文献

Fas-mediated apoptosis is a major player of many physiological and pathological cellular processes. Fas-regulated immune regulation exhibits either the beneficial or the harmful effects which is associated with the onset or development of immune disorders. Alterations in apoptosis may contribute to age-associated changes. However, the role of apoptosis in the ageing process remains ambiguous. Here we demonstrated Fas signaling-mediated premature senescence in young mouse embryonic fibroblast (MEF) cells. Activated Fas signaling by agonist Jo-2 resulted in declined senescence in young and aged MEFs. Premature senescence induced the early activation of senescence markers, including the increase in the percentage of SA-β-galactosidase (SA-β-gal) cells, the induction of p53 phosphorylation, and the enhanced expression of p16 and p21 protein and elevated IL-6 pro-inflammatory cytokine in the absence of Fas. The elevated production of reactive oxygen species (ROS) in Fas-deficient MEFs was associated with dysfunctional mitochondria. Further, we determined that the known ROS scavenger NAC (N-acetyl-l-cysteine) could reverse the process of premature senescence in absence of Fas. Therefore, this study signifies a novel role of Fas in the control of cellular senescence. Absence of Fas signaling led to premature cellular senescence, which was significantly reduced by Fas agonist Jo-2 . Young Fas knock out (FasKO) MEF cells exhibit enhanced SA-β-gal activity, p16, p21, p53, pP38 and IGFBP5. Young FasKO cells display elevated inflammatory IL-6. Young FasKO MEF cells produced significantly higher ROS and defect in mitochondrial function. ROS scavenger NAC (N-acetyl-l-cysteine) could reverse the process of premature aging in absence of Fas.
DOI: 10.1371/journal.pone.0154516
发表时间: 2016
期刊: PloS one
影响因子: 3.7
作者:
Balestro E;Calabrese F;Turato G;Lunardi F;Bazzan E;Marulli G;Biondini D;Rossi E;Sanduzzi A;Rea F;Rigobello C;Gregori D;Baraldo S;Spagnolo P;Cosio MG;Saetta M
通讯作者: Saetta M
DOI: 10.1002/1873-3468.13498
发表时间: 2019-07-01
期刊: FEBS LETTERS
影响因子: 3.5
作者:
Chapman, James;Fielder, Edward;Passos, Joao F.
通讯作者: Passos, Joao F.
DOI: 10.1016/j.ymeth.2016.06.008
发表时间: 2016-10-15
期刊: METHODS
影响因子: 4.8
作者:
Oparka, Monika;Walczak, Jaroslaw;Wieckowski, Mariusz R.
通讯作者: Wieckowski, Mariusz R.
衰老中的细胞衰老:从机制到治疗机会。
DOI: 10.1038/s41580-020-00314-w
发表时间: 2021-03
期刊: Nature reviews. Molecular cell biology
影响因子: --
作者:
Di Micco R;Krizhanovsky V;Baker D;d'Adda di Fagagna F
通讯作者: d'Adda di Fagagna F
DOI: 10.1371/journal.pbio.0060301
发表时间: 2008-12-02
期刊: PLoS biology
影响因子: 9.8
作者:
Coppé JP;Patil CK;Rodier F;Sun Y;Muñoz DP;Goldstein J;Nelson PS;Desprez PY;Campisi J
通讯作者: Campisi J