Sirtuin1缺乏可加剧内质网应激下黑素细胞凋亡。

IF 4.5 2区 医学 Q2 CELL BIOLOGY
Jing Zhu, Youming Guo, Lingling Luo, Xin Huang, Tianqi Wei, Baiyi Zuo, Guanying Liu, Wenbo Bu, Chengrang Li
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引用次数: 0

摘要

白癜风是一种由黑色素细胞被靶向破坏而引起的色素脱失性疾病,导致皮肤和头发色素脱失,并产生显著的心理压力。然而,其发生和发展的机制尚不清楚。内质网应激与氧化应激和自身免疫有关,参与白癜风的发生,内质网应激延长可诱导细胞凋亡。Sirt1可能是内质网应激的关键调节因子。因此,我们在体外和体内研究了Sirt1如何调节内质网应激诱导的黑素细胞凋亡。我们的研究结果表明Sirt1影响内质网应激诱导的黑素细胞凋亡。Sirt1抑制加重了小鼠白癜风表型;从而防止应激反应,并减少未折叠蛋白反应。这些结果提示Sirt1损伤可加速白癜风黑素细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sirtuin1 Deficiency Could Exacerbate Melanocyte Apoptosis Under Endoplasmic Reticulum Stress.

Vitiligo is a depigmentation disease caused by the targeted destruction of melanocytes, resulting in skin and hair depigmentation and significant psychological stress. However, the mechanisms underlying its onset and progression remain unclear. Endoplasmic reticulum (ER) stress, which is linked with oxidative stress and autoimmunity, is involved in the development of vitiligo, and prolonged ER stress induces apoptosis. Sirtuin 1 (Sirt1) might be a key regulator of ER stress. Thus, we explored how Sirt1 modulates ER stress-induced melanocyte apoptosis in vitro and in vivo. Our results showed that Sirt1 affected ER stress-induced apoptosis of melanocyte apoptosis when upon to ER stress in vitro. Sirt1 inhibition aggravated the vitiligo phenotype in mice; thereby protecting against the stress response, and abating the unfolded protein response. These results suggest that Sirt1 impairment could accelerate melanocyte apoptosis in vitiligo.

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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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