MiR-101 regulates apoptosis of trophoblast HTR-8/SVneo cells by targeting endoplasmic reticulum (ER) protein 44 during preeclampsia

被引:57
作者
Zou, Y. [1 ]
Jiang, Z. [1 ]
Yu, X. [2 ]
Zhang, Y. [1 ]
Sun, M. [2 ]
Wang, W. [1 ]
Ge, Z. [1 ]
De, W. [2 ]
Sun, L. [1 ]
机构
[1] Nanjing Med Univ, Dept Obstet & Gynecol, Affiliated Hosp 1, Nanjing 210000, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Biochem & Mol Biol, Nanjing 210000, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
ANTIANGIOGENIC FACTORS; OXIDATIVE STRESS; MICRORNAS; PREGNANCY; MIRNAS; PATHOPHYSIOLOGY; PROLIFERATION; PATHOGENESIS; MIGRATION; RISK;
D O I
10.1038/jhh.2014.35
中图分类号
R6 [外科学];
学科分类号
100210 [外科学];
摘要
To investigate a possible association between miR-101 and apoptosis of human trophoblast cells mediated by endoplasmic reticulum protein 44 (ERp44) in preeclampsia (PE), we explored the expression of miR-101 in PE placentas (n = 30) compared with normotensive pregnant placentas (n = 30) and the correlation between miR-101 and ERp44 was also analyzed. Furthermore, both the apoptotic rate of trophoblast cells and the ER stress-induced apoptotic proteins were assayed when the HTR-8/SVneo cells were treated with miR-101 mimics or inhibitors in vitro. We found a lower expression of miR-101 and an inverse correlation between miR-101 and ERp44 protein in PE placentas. Upregulation of miR-101 expression could inhibit trophoblast HTR-8/SVneo cell apoptosis and repress ER stress-induced apoptotic proteins by targeting ERp44 in vitro, whereas inhibition of miR-101 could induce HTR-8/SVneo cell apoptosis. Our findings indicated that overexpression of miR-101 could downregulate ERp44 and suppress apoptosis in trophoblast cells during PE. Therefore, loss of miR-101 expression could contribute to ER stress-induced trophoblast cell apoptosis by targeting ERp44.
引用
收藏
页码:610 / 616
页数:7
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