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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Induction of cellular senescence by secretory phospholipase A2 in human dermal fibroblasts through an ROS-mediated p53 pathway.
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Induction of cellular senescence by secretory phospholipase A2 in human dermal fibroblasts through an ROS-mediated p53 pathway.

机译：通过ROS介导的p53途径在人皮肤成纤维细胞中由分泌磷脂酶A2诱导细胞衰老。

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摘要

Secretory phospholipase A(2) (sPLA(2)) is involved in various cellular physiological and pathological responses, especially in inflammatory responses. Accumulating evidence suggests that inflammation is an underlying basis for the molecular alterations that link aging and age-related pathological processes. However, the involvement of sPLA(2) in cellular senescence is not clear. In this study, we found that sPLA(2) treatment induces cellular senescence in human dermal fibroblasts (HDFs), as confirmed by increases in senescence-associated beta-galactosidase activity, changes in cell morphology, and upregulation of p53/p21 protein levels. sPLA(2)-induced senescence was observed in p16-knockdown HDFs and p16-null mouse fibroblasts, but not in p53-knockdown HDFs and p53-null mouse fibroblasts. Treatment with sPLA(2) increases reactive oxygen species (ROS) production, and an antioxidant, N-acetylcysteine, inhibits sPLA(2)-induced cellular senescence. These results suggest that sPLA(2) has a role in cellular senescence in HDFs during inflammatory response by promoting ROS-dependent p53 activation and might therefore contribute to inflammatory disorders associated with aging.
机译：分泌型磷脂酶A（2）（sPLA（2））参与各种细胞生理和病理反应，尤其是炎症反应。越来越多的证据表明，炎症是联系衰老和与年龄相关的病理过程的分子变化的基础。但是，尚不清楚sPLA（2）是否参与细胞衰老。在这项研究中，我们发现sPLA（2）处理可诱导人类皮肤成纤维细胞（HDF）的细胞衰老，这一点已被衰老相关的β-半乳糖苷酶活性增加，细胞形态变化和p53 / p21蛋白水平上调所证实。 sPLA（2）诱导衰老观察到p16基因敲低HDFs和p16 null小鼠成纤维细胞，但在p53基因敲低HDFs和p53 null小鼠成纤维细胞中则没有。 sPLA（2）的治疗可增加活性氧（ROS）的产生，抗氧化剂N-乙酰半胱氨酸可抑制sPLA（2）诱导的细胞衰老。这些结果表明，sPLA（2）在炎症反应过程中通过促进ROS依赖的p53活化而在HDFs细胞衰老中起作用，因此可能导致与衰老相关的炎症。

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