Downregulation of FHL2 suppressed trophoblast migration, invasion and epithelial–mesenchymal transition in recurrent miscarriage

滋养层 上皮-间质转换 基因敲除 细胞迁移 生物 波形蛋白 癌症研究 小干扰RNA 庆大霉素保护试验 下调和上调 免疫印迹 男科 转染 细胞 免疫学 胎盘 细胞培养 医学 胎儿 免疫组织化学 基因 怀孕 生物化学 遗传学
作者
Xiaorui Luan,Junyu Zhai,Shang Li,Yanzhi Du
出处
期刊:Reproductive Biomedicine Online [Elsevier BV]
卷期号:: 103342-103342
标识
DOI:10.1016/j.rbmo.2023.103342
摘要

Is four and a half LIM domain 2 (FHL2) involved in trophoblast migration, invasion and epithelial-mesenchymal transition (EMT) in recurrent miscarriage?Villus tissue was collected from 24 patients who had experienced recurrent miscarriage and 24 healthy controls. FHL2 mRNA and protein expression in villus specimens were observed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Small interfering RNA and overexpression plasmid were used to change the FHL2 expression. JAR and HTR8/SVneo cell lines were used to conduct scratch-wound assay and transwell assay to detect trophoblast migration and invasion of FHL2. Downstream molecule expression of mRNA and protein and EMT markers were verified by qRT-PCR and Western blot.Significantly lower FHL2 mRNA (P = 0.019) and protein (P = 0.0014) expression was found in trophoblasts from the recurrent miscarriage group compared with healthy controls. FHL2 knockdown repressed migration (P = 0.0046), invasion (P < 0.001) and EMT, as shown by significant differences in mRNA and protein expression of the EMT markers N-cadherin, E-cadherin, Vimentin and Snail (all P < 0.05) of extravillus trophoblasts. FHL2 overexpression enhanced migration (P = 0.025), invasion (P < 0.001) and EMT of extravillus trophoblasts (all EMT markers P < 0.05). The positive upstream factor FHL2 in the extracellular signal-related kinase pathway induced JunD expression, thereby promoting trophoblast migration and invasion via matrix metalloproteinase 2.FHL2 is involved in a regulatory pathway of trophoblast migration, invasion and EMT during early pregnancy, and may have a role in recurrent miscarriage pathogenesis, which can serve as a possible target for novel therapeutic development.
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