下调和上调
海马结构
信号转导
磷酸化
细胞生物学
化学
细胞色素c
细胞凋亡
线粒体
胞浆
分子生物学
生物
生物化学
内分泌学
酶
基因
作者
Zheng Wang,Xiang Han,Mei Cui,Kun Fang,Zhengyu Liu,Qiang Dong
摘要
We have documented that tissue kallikrein (TK) prevents neurons from hypoxia/reoxygenation injury through the B2R‐ERK1/2 pathway and the antihypoxic function of TK through Homer1b/c‐ERK1/2 signaling pathways. The present study investigates the molecular mechanisms of exogenous TK activation of the B2R‐ERK1/2 pathway through the β‐arrestin‐2 assembled B2R‐Raf‐MEK1/2 signaling module in vivo. The cresyl violet staining results indicated that exogenous TK protected the rat hippocampal CA1 neurons against cerebral ischemia/reperfusion (I/R) injury. The immunoprecipitation (IP) and immunoblotting (IB) results revealed that exogenous TK upregulated the β‐arrestin‐2 assembled B2R‐Raf‐MEK1/2 signaling module and upregulated the phosphorylation of Raf (p‐Raf), MEK1/2 (p‐MEK1/2), and ERK1/2 (p‐ERK1/2). Meanwhile, exogenous TK upregulated the expression of nuclear factor‐κB (NF‐κB), depressed the release of cytochrome c (Cyt c) and bax from mitochondria to the cytosol, and depressed the activation of caspase‐3. Take together, our results suggest that exogenous TK attenuated the cerebral I/R induced rat hippocampal CA1 neurons injury through activating the β‐arrestin‐2 assembled B2R‐Raf‐MEK1/2 signaling module and that the activated B2R‐Raf‐MEK1/2 signaling module could upregulate the expression of NF‐κB, decrease the release of cytochrome c and bax from mitochondria to the cytosol, and depress the activation of caspase‐3. © 2014 Wiley Periodicals, Inc.
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