Elevated microRNA-141-3p in placenta of non-diabetic macrosomia regulate trophoblast proliferation
Publication date: Available online 9 November 2018
Author(s): Dan Guo, Hua Jiang, Yiqiu Chen, Jing Yang, Ziqiang Fu, Jing Li, Xiumei Han, Xian Wu, Yankai Xia, Xinru Wang, Liping Chen, Qiuqin Tang, Wei Wu
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.
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.
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.
miR-141-3p could stimulate placental cell proliferation to participate in the occurrence and development of NDFMS.