Abstract
Missed abortion is a peculiar form of spontaneous abortion before 20 weeks' gestation. The definite etiology and pathogenesis are not fully understood. Recent studies have demonstrated that p53/Mdm2-mediated ubiquitination of the IGF-1R may be closely related to G-protein-coupled receptor kinases (GRK)/β-arrestin1 system. Our previous studies have confirmed that the elevated expression of p53 and Mdm2 may be responsible for apoptosis during missed abortion. However, there was no information surrounding β-arrestin1 in missed abortion. The mRNA levels of β-arrestin1 in villous samples of 30 missed abortion patients and 31 healthy controls were determined by real-time quantitative polymerase chain reaction (PCR). Immunohistochemistry was used to explore the expression and location of β-arrestin1, p53, Mdm2, VEGF and HIF-lα in trophoblasts. Transwell assays were performed to examine the influences of β-arrestin1 expression on cell invasion. Furthermore, we tested the effect of β-arrestin1 on the expression of p53, Mdm2, ERK, AKT and NF-κB. The expression of β-arrestin1 in the villous samples of missed abortion group was dramatically lower than control group by quantitative real-time-PCR and immunohistochemistry. Furthermore, the patients with missed abortion showed significantly higher levels of p53, Mdm2, HIF-lα and lower level of VEGF than healthy controls by immunohistochemistry. Functional studies showed that suppression of β-arrestin1 in HTR-8 cells inhibited cell invasion. The protein expressions of ERK and AKT in HTR-8 cells were significantly downregulated by reducing the expression of β-arrestin1, while the expressions of p53, Mdm2, NF-κB were enhanced. Overexpression of β-arrestin1 exhibited the adverse effect. Our data indicated that β-arrestin1 play an important role in maintaining the maternal-fetal tolerance, the decreased expression of β-arrestin1 in the villous samples may be related with the development of missed abortion.
Highlights
Missed abortion is a peculiar form of spontaneous abortion before 20 weeks’ gestation, which is characterized by the unrecognized intrauterine death of the embryo or fetus without outside intervention[1]
Recent studies have demonstrated that p53/Mdm2-mediated ubiquitination of the IGF-1R maybe closely related to G protein-coupled receptor kinases (GRK)/β-arrestin1 system
Our data indicated that β-arrestin1 could play an important role in maintaining the maternal-fetal tolerance, the decreased β-arrestin1 expression in the villous samples may be related to the development of missed abortion
Summary
Missed abortion is a peculiar form of spontaneous abortion before 20 weeks’ gestation, which is characterized by the unrecognized intrauterine death of the embryo or fetus without outside intervention[1]. The definite etiology and pathogenesis are not fully understood, many studies have shown that cell apoptosis play a key role in missed abortion. Trophoblast cell apoptosis was observed to be a appropriate extent which facilitate the formation and development of villi and chorionic villi branch. Identifying and characterizing key molecular markers involved in missed abortion are important for developing new therapeutic treatments. Missed abortion is a nonviable pregnancy before the 20th week of gestation with retained products of conception. Recent studies have demonstrated that p53/Mdm2-mediated ubiquitination of the IGF-1R maybe closely related to G protein-coupled receptor kinases (GRK)/β-arrestin system. Our previous studies have confirmed that the elevated expression of p53 and Mdm may be responsible for apoptosis during missed abortion. There was no information surrounding β-arrestin in missed abortion
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