分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

Effect of the p53–tristetraprolin–stathmin-1 pathway on trophoblasts at maternal–fetal interface

Xiao-Ling Ma, Xiao-Cui Li, Fu-Ju Tian, Si-Ming Zhang, Xiao-Rui Liu, Yan Zhang, Jian-Xia Fan, Yi Lin

Journal:PLoS One

IF:2.81

DOI:10.1371/journal.pone.0179852

PMID:28658321

Published:2017-06-28

research field:分子生物学细胞生物学妇产科学

Abstract

Problem To reveal the effect of p53–tristetraprolin–stathmin-1 signaling on trophoblasts and recurrent spontaneous abortion (RSA). Method of study Stathmin-1 (STMN1), p53, and tristetraprolin (TTP) expression in paraffin-embedded villus tissue was determined using immunohistochemistry. HTR-8/SVneo cells were treated with doxorubicin to activate p53; STMN1 and TTP levels were detected by quantitative reverse transcription–PCR and western blotting. Western blotting and immunofluorescence were used to investigate STMN1 expression after TTP overexpression or knockdown in HTR-8 cells. Results STMN1 was downregulated and p53 was upregulated in the villus tissue from patients with RSA. Doxorubicin decreased STMN1 expression but enhanced TTP expression in HTR-8 cells. In vitro , TTP overexpression inhibited STMN1 production; TTP knockdown promoted it. TTP downregulated STMN1 expression in trophoblasts by directly binding its 3ʹ untranslated region. Conclusions TTP modulates trophoblast function and interacts with STMN1 and p53, and is related to pregnancy outcomes.

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