ArticleScientific reports2026
A miR-200b-Filamin A axis drives epicardial contribution to cardiogenesis.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The epicardium provides essential cellular and molecular cues required for proper cardiogenesis and cardiac repair. Epicardial-derived cells (EPDCs) play a pivotal role in establishing cardiac structure, contributing to coronary vasculature formation, connective tissue organization, and post-ischemic cardiac remodeling. During EPDC emergence, the epicardium must preserve a precise balance between cellular motility and epithelial integrity. However, the mechanisms determining why some epicardial cells undergo epithelial-to-mesenchymal transition to become EPDCs while others retain an epithelial state remain unclear. We show that miR-200b is expressed in a subset of epicardial cells during embryonic EPDC formation. Gain-and loss-of-function experiments reveal that miR-200b regulates the overall number of EPDCs by modulating the proportion of symmetric and asymmetric cell divisions. RNA pull-down coupled with RNA-seq, together with in vitro and ex vivo functional assays, identified filamin A (FLNA)-a key regulator of spindle positioning during asymmetric division-as a direct miR-200b target in epicardial cells. FLNA loss reduced asymmetric divisions, supporting its role in promoting this division mode. Overall, our study defines a miR-200b-FLNA axis that governs symmetric versus asymmetric division to control epicardial tissue dynamics during cardiogenesis. Additionally, altered miR-200b expression after myocardial infarction in mice and humans suggests a potential role post-MI.
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