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<p>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.</p>

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A miR-200b–Filamin A axis drives epicardial contribution to cardiogenesis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月26日

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  • Cristina Sánchez-Fernández,
  • Carlos García-Padilla,
  • Estefanía Lozano-Velasco,,
  • Francisco Hernandez-Torres,
  • Óscar Ocaña,
  • Ana Quintas,
  • Enrique Vázquez,
  • Laura Alonso-Herranz,
  • Mercedes Ricote,
  • Beatriz Román-Payan,
  • Rita Carmona,
  • Diego Franco,
  • Jorge N. Domínguez,
  • Amelia E. Aránega

摘要

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.