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2-氯乙醇通过丝裂原活化蛋白激酶信号通路诱导原代培养大鼠星形胶质细胞中基质金属蛋白酶-2的上调。

2-Chloroethanol Induced Upregulation of Matrix Metalloproteinase-2 in Primary Cultured Rat Astrocytes Via MAPK Signal Pathways.

作者信息

Sun Qi, Liao Yingjun, Wang Tong, Tang Hongge, Wang Gaoyang, Zhao Fenghong, Jin Yaping

机构信息

Department of Occupational and Environmental Health, School of Public Health, China Medical University Shenyang, China.

Department of Physiology, China Medical University Shenyang, China.

出版信息

Front Neurosci. 2017 Jan 4;10:593. doi: 10.3389/fnins.2016.00593. eCollection 2016.

DOI:10.3389/fnins.2016.00593
PMID:28101000
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5209348/
Abstract

This study was to explore the mechanisms underlying 1,2-dichloroethane (1,2-DCE) induced brain edema by focusing on alteration of matrix metalloproteinase-2 (MMP-2) in rat astrocytes induced by 2-chloroethanol (2-CE), an intermediate metabolite of 1,2-DCE . Protein and mRNA levels of MMP-2, and the phosphorylated protein levels of p38 MAPK (p-p38), extracellular signal regulated protein kinase (p-ERK1/2) and c-Jun N-terminal kinase (p-JNK1/2) in astrocytes were examined by immunostaining, western blot or real-time RT-PCR analysis. Findings from this study disclosed that protein levels of MMP-2 were upregulated by 2-CE in astrocytes. Meanwhile, protein levels of p-p38, p-ERK1/2 and p-JNK1/2 were also increased apparently in the cells treated with 2-CE. Moreover, pretreatment of astrocytes with SB202190 (inhibitor of p38 MAPK), U0126 (inhibitor of ERK1/2) or SP600125 (inhibitor of JNK1/2) could suppress the upregulated expression of p-p38, p-ERK1/2, and p-JNK1/2. In response to suppressed protein levels of p-p38 and p-JNK1/2, the protein levels of MMP-2 also decreased significantly, indicating that activation of MAPK signal pathways were involved in the mechanisms underlying 2-CE-induced upregulation of MMP-2 expression.

摘要

本研究旨在通过关注1,2 - 二氯乙烷（1,2 - DCE）的中间代谢产物2 - 氯乙醇（2 - CE）诱导大鼠星形胶质细胞中基质金属蛋白酶 - 2（MMP - 2）的变化，探索1,2 - 二氯乙烷诱导脑水肿的机制。通过免疫染色、蛋白质印迹或实时逆转录 - 聚合酶链反应分析检测星形胶质细胞中MMP - 2的蛋白质和mRNA水平，以及p38丝裂原活化蛋白激酶（p - p38）、细胞外信号调节蛋白激酶（p - ERK1/2）和c - Jun氨基末端激酶（p - JNK1/2）的磷酸化蛋白水平。本研究结果表明，2 - CE可使星形胶质细胞中MMP - 2的蛋白质水平上调。同时，在用2 - CE处理的细胞中，p - p38、p - ERK1/2和p - JNK1/2的蛋白质水平也明显增加。此外，用SB202190（p38丝裂原活化蛋白激酶抑制剂）、U0126（ERK1/2抑制剂）或SP600125（JNK1/2抑制剂）预处理星形胶质细胞可抑制p - p38、p - ERK1/2和p - JNK1/2的上调表达。响应于p - p38和p - JNK1/2蛋白质水平的抑制，MMP - 2的蛋白质水平也显著降低，表明丝裂原活化蛋白激酶信号通路的激活参与了2 - CE诱导的MMP - 2表达上调的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/fd3d4957c0af/fnins-10-00593-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/10d36eb5b697/fnins-10-00593-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/42c99a11b3c6/fnins-10-00593-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/a97ae264e870/fnins-10-00593-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/d98ea9f1d613/fnins-10-00593-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/fd3d4957c0af/fnins-10-00593-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/10d36eb5b697/fnins-10-00593-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/42c99a11b3c6/fnins-10-00593-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/a97ae264e870/fnins-10-00593-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/d98ea9f1d613/fnins-10-00593-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2b1/5209348/fd3d4957c0af/fnins-10-00593-g0005.jpg

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