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首页> 外文期刊>EBioMedicine >Elevated microRNA-141-3p in placenta of non-diabetic macrosomia regulate trophoblast proliferation
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Elevated microRNA-141-3p in placenta of non-diabetic macrosomia regulate trophoblast proliferation

机译：非糖尿病性巨大儿胎盘中的microRNA-141-3p升高调节滋养细胞增殖

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Background Several studies have reported microRNAs (miRNAs) could regulate the placental development, though the role and mechanism of miRNAs in the development of non-diabetic macrosomia (NDFMS) remains unclear. Methods To identify the aberrantly expressed key miRNAs in placenta of NDFMS, we employed a strategy consisting of initial screening with miRNA microarray and further validation with quantitative RT-PCR assay (qRT-PCR). In vitro cellular model and a mouse pregnancy model were used to delineate the functional effects of key miRNA on proliferation, invasion, and migration. Findings miR-141-3p was identified as the key miRNA with expression level significantly higher in placentas of NDFMS compared with those from normal controls. Overexpressed miR-141-3p in HTR-8/SVneo cells contributed to increased cell proliferation, invasion, and migration. miR-141-3p inhibition in HTR-8/SVneo cells resulted in decreased cell proliferation and invasion. Significantly increased infant birth weight was observed in late pregnancy of C57BL/6J mice treated with miR-141-3p agomir. However, no significant difference was found in early pregnancy of C57BL/6J mice treated with miR-141-3p agomir. Interpretation miR-141-3p could stimulate placental cell proliferation to participate in the occurrence and development of NDFMS.
机译：背景几项研究报告了microRNA（miRNA）可以调节胎盘的发育，尽管miRNA在非糖尿病性巨人症（NDFMS）发育中的作用和机制尚不清楚。方法为了鉴定NDFMS胎盘中异常表达的关键miRNA，我们采用了一种策略，包括用miRNA芯片进行初步筛选，再用定量RT-PCR分析（qRT-PCR）进行验证。使用体外细胞模型和小鼠妊娠模型来描述关键miRNA对增殖，侵袭和迁移的功能作用。发现miR-141-3p是关键的miRNA，与正常对照组相比，其在NDFMS胎盘中的表达水平明显更高。 HTR-8 / SVneo细胞中过表达的miR-141-3p导致细胞增殖，侵袭和迁移增加。 HTR-8 / SVneo细胞中的miR-141-3p抑制导致细胞增殖和侵袭减少。在用miR-141-3pagomir治疗的C57BL / 6J小鼠的晚期妊娠中观察到婴儿出生体重显着增加。但是，在用miR-141-3pagomir治疗的C57BL / 6J小鼠的早期妊娠中未发现明显差异。解释miR-141-3p可以刺激胎盘细胞增殖，参与NDFMS的发生和发展。

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