Abstract
ProblemTo reveal the effect of p53–tristetraprolin–stathmin-1 signaling on trophoblasts and recurrent spontaneous abortion (RSA).Method of studyStathmin-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.ResultsSTMN1 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.ConclusionsTTP modulates trophoblast function and interacts with STMN1 and p53, and is related to pregnancy outcomes.
Highlights
Miscarriage, the most common complication of pregnancy, is defined as the spontaneous loss of pregnancy before the fetus has reached viability [1]
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
The cells were harvested at 6 h, 12 h, and 24 h after treatment. mRNA was analyzed by quantitative real-time PCR; proteins were analyzed by western blotting and immunofluorescence
Summary
Miscarriage, the most common complication of pregnancy, is defined as the spontaneous loss of pregnancy before the fetus has reached viability [1]. Recurrent spontaneous abortion (RSA) is defined as the occurrence of two or more consecutive pregnancy losses before 24 weeks of gestation [2]. Stathmin-1 (STMN1), referred to as OP18, is a ubiquitous cytosolic phosphoprotein, proposed to be a small regulatory protein and a relay integrating diverse intracellular signaling pathways involved in controlling cell proliferation, differentiation, and activities [10]. Recent reports have shown differential STMN1 expression in human endometrial and placental cells and that it may participate in decidualization. We found that STMN1 was downregulated in the chorionic villi from patients with RSA. It is a trophoblast proliferation- and invasion-associated microtubule regulatory protein that participates in the pathogenesis of RSA [12]
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