Abstract
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 influences β-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 alters β-catenin expression,critically influencing the EMT process in the embryonic epicardial cells via the cell adhesion mechanism.
基金项目
Key Project of Technology Innovation and Application Development in Chongqing(CSTB2023TIAD-KPX0048)
Construction of Graduate Tutor Team in Chongqing Medical University(cqmudstd202205)
国家自然科学基金青年科学基金(81800254)
Postdoctoral Project of Chongqing Natural Science Foundation(CSTB2022NSCQ-BHX0626)
国家科技期刊平台
NSTL
万方数据