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MiR-135b-5p targets ADAM12 to suppress invasion and accelerate trophoblast apoptosis in preeclampsia

滋养层 子痫前期 下调和上调 微泡 细胞凋亡 转染 小RNA 细胞滋养层 男科 细胞生物学 胎盘 生物 细胞培养 化学 医学 怀孕 基因 胎儿 遗传学
作者
Bo Sun,Taotao Jiang,Jiaxi Yong,Julan Peng,Shangkun Dong,Yanli Gu,Xinmei Ji,Liqiong Luo,Wen-Lin Chang
出处
期刊:Placenta [Elsevier]
卷期号:143: 69-79
标识
DOI:10.1016/j.placenta.2023.10.004
摘要

Preeclampsia was a serious complication often leaded to adverse pregnancy outcomes. Abnormal placental miR-135b-5p expression in preeclampsia was observed in our preliminary investigation. However, the role of miR-135b-5p in preeclampsia was unclear. We determined the miR-135b-5p expression pattern at the fetomaternal interface and levels in placental tissue and exosomes. MiR-135b-5p expression in the trophoblast cell line HTR8/SVneo was manipulated by transient agomir or antagomir transfection or establishment of HTR8/SVneo cell line stably overexpressing miR-135b or miR-135b-5p-sponger. Then the function of miR-135b-5p on the motility of HTR8/SVneo cells, and its effects on cell viability was determined. Finally, we confirmed the relationship between miR-135b-5p and ADAM12. MiR-135b-5p exclusively expressed in the villous cytotrophoblast, and extravillous trophoblast. Significant miR-135b-5p upregulation was observed in the placenta and peripheral plasma exosomes in preeclampsia, and could be a highly sensitive molecular marker for preeclampsia. Elevated miR-135b-5p expression significantly promoted apoptosis and inhibited HTR8/SVneo cell invasion and migration. Binding of miR-135b-5p to the ADAM12 mRNA 3ʹ-untranslated region was predicted by bioinformatics analysis and confirmed using a dual-luciferase reporter assay. High miR-135-5p levels inhibit the invasion and migration of trophoblastic cells, possibly by directly binding to the 3ʹ-UTR of DADM12 and suppressing its translation efficiency, thereby nullifying the promotion of trophoblast invasion and migration via ADAM12. Abnormal upregulation of miR-135b-5p may be involved in preeclampsia through triggering trophoblast apoptosis and impeding trophoblast invasion and migration by targeting ADAM12.
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