miR-194-3p regulates epithelial-mesenchymal transition in embryonic epicardial cells via p120/β-catenin signaling  

作　　者：Tianhua Xiong Dinghui Wang Huiping Yang Bin Liu Yingrui Li Wenlong Yu Jing Wang Qiang She 

机构地区：[1]Department of Cardiology,The Second Affiliated Hospital of Chongqing Medical University,Chongqing 400010,China

出　　处：《Acta Biochimica et Biophysica Sinica》2024年第5期717-729,共13页生物化学与生物物理学报（英文版）

基　　金：supported by the grants from the Key Project of Technology Innovation and Application Development in Chongqing(No.CSTB2023TIAD-KPX0048);the Construction of Graduate Tutor Team in Chongqing Medical University(No.cqmudstd202205);the National Natural Science Foundation of China Youth Science Fund Project(No.81800254);the Postdoctoral Project of Chongqing Natural Science Foundation(No.CSTB2022NSCQ-BHX0626).

摘　　要：The epicardium is integral to cardiac development and facilitates endogenous heart regeneration and repair.While miR-194-3p is associated with cellular migration and invasion,its impact on epicardial cells remains uncharted.In this work we use gain-of-function and loss-of-function methodologies to investigate the function of miR-194-3p in cardiac development.We culture embryonic epicardial cells in vitro and subject them to transforming growth factorβ(TGF-β)treatment to induce epithelial-mesenchymal transition(EMT)and monitor miR-194-3p expression.In addition,the effects of miR-194-3p mimics and inhibitors on epicardial cell development and changes in EMT are investigated.To validate the binding targets of miR-194-3p and its ability to recover the target gene-phenotype,we produce a mutant vector p120-catenin-3′UTR-MUT.In epicardial cells,TGF-β-induced EMT results in a notable overexpression of miR-194-3p.The administration of miR-194-3p mimics promotes EMT,which is correlated with elevated levels of mesenchymal markers.Conversely,miR-194-3p inhibitor attenuates EMT.Further investigations reveal a negative correlation between miR-194-3p and p120-catenin,which influencesβ-catenin level in the cell adhesion pathway.The suppression of EMT caused by the miR-194-3p inhibitor is balanced by silencing of p120-catenin.In conclusion,miR-194-3p directly targets p120-catenin and modulates its expression,which in turn altersβ-catenin expression,critically influencing the EMT process in the embryonic epicardial cells via the cell adhesion mechanism.

关 键 词：embryonic epicardial cells epithelial-mesenchymal transition development miR-194-3p P120-CATENIN 

分 类 号：R321[医药卫生—人体解剖和组织胚胎学]