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卵泡抑素样蛋白 3 与子痫前期的关系。

Involvement of follistatin-like 3 in preeclampsia.

机构信息

Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, China; Key Laboratory of Women's Reproductive Health of Zhejiang Province, Hangzhou, China; Key Laboratory of Reproductive Genetics of the Ministry of Education, Hangzhou, China.

出版信息

Biochem Biophys Res Commun. 2018 Nov 30;506(3):692-697. doi: 10.1016/j.bbrc.2018.10.139. Epub 2018 Oct 27.

DOI:10.1016/j.bbrc.2018.10.139
PMID:30454705
Abstract

INTRODUCTION

Preeclampsia is a main cause of maternal and perinatal mortality and morbidity. The expression of follistatin-like 3 (FSTL3) is enhanced in maternal serum and placenta of preeclamptic women. However, whether FSTL3 is involved in the pathophysiologic of preeclampsia has not been clarified yet.

METHOD

Trophoblast cell lines Swan71 and JAR cells were cultured and siRNA was used to silence FSTL3. The expression of FSTL3 was determined by Western blotting. The matrigel-coated transwell and wound healing assays were used to assess invasion and migration, cell proliferation and apoptosis were detected by CCK-8 and flow cytometric analysis, respectively. Oil red O staining was used to detect the lipid storage in trophoblast.

RESULTS

Hypoxia culture significantly enhanced the expression of FSTL3 by trophoblast. Down-regulation of FSTL3 significantly suppressed the proliferation, migration, invasion and lipid storage but increased apoptosis of trophoblast.

DISCUSSION

Aberrant expression of FSTL3 in preeclampsia led to the dysfunction of trophoblast, indicating its involvement in the pathogenesis of preeclampsia.

摘要

简介

子痫前期是孕产妇和围生儿发病率和死亡率的主要原因。在子痫前期妇女的母血清和胎盘组织中,卵泡抑素样蛋白 3(FSTL3)的表达增强。然而,FSTL3 是否参与子痫前期的病理生理过程尚未阐明。

方法

培养胎盘滋养层细胞系 Swan71 和 JAR 细胞,并使用 siRNA 沉默 FSTL3。通过 Western blot 检测 FSTL3 的表达。用基质胶包被的 Transwell 和划痕愈合实验评估侵袭和迁移,通过 CCK-8 和流式细胞术分析分别检测细胞增殖和凋亡,油红 O 染色检测滋养层中的脂质储存。

结果

缺氧培养显著增强了滋养层中 FSTL3 的表达。下调 FSTL3 显著抑制了滋养层的增殖、迁移、侵袭和脂质储存,但增加了滋养层的凋亡。

讨论

子痫前期中 FSTL3 的异常表达导致了滋养层功能障碍,表明其参与了子痫前期的发病机制。

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