GSNO引起过氧化物酶-2亚硝基化经由XBP-1s/PI3K 通路促小鼠胚胎干细胞分化心肌
GSNO引起过氧化物酶-2亚硝基化经由XBP-1s/PI3K 通路促小鼠胚胎干细胞分化心肌
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DOI：
10.1016/j.freeradbiomed.2016.05.025
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Yijia Lou
中科院分区：
文献类型：
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作者：
Bowen Wu;Hao Yu;Yifan Wang;Zongfu Pan;Yihan Zhang;Lijun Ge;Xin Huang;Yijia Lou
Protein nitrosylation is a ubiquitous post-translational modification in almost all biological systems. However, its function on stem cell biology is so far incompletely understood. Here, we demonstrated that peroxiredoxin 2 (Prdx-2) nitrosylation was involved in cardiomyocyte differentiation of mouse embryonic stem (ES) cells induced byS-nitrosoglutathione (GSNO). We found that temporary GSNO exposure could promote ES cell-derived cardiomyogenesis. Using a stable isotope labeling by amino acids in cell culture (SILAC)-based proteomics approach, coupled with biotin switch technique, a total of 104 nitrosylated proteins were identified. Specifically, one of the antioxidant enzymes, Prdx-2, was abundantly nitrosylated and temporarily reduced in antioxidant activity, causing transient endogenous hydrogen peroxide (H2O2) accumulation and subsequent X-box binding protein-1s/phosphatidylinositol 3-kinase pathway activation. The present study reveals the mechanism in which GSNO favors cardiomyocyte differentiation. Prdx-2 nitrosylation could be a potent strategy to affect the pluripotent stem cell-derived cardiomyogenesis.
