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The Molecular Brake: Piezo1 Activation Delays Epithelial Gap Closure Through Transcriptional Downregulation of Adhesion Machinery

ABSTRACT: The mechanosensitive ion channel Piezo1 is a critical regulator of epithelial homeostasis, influencing processes such as proliferation, extrusion, and wound healing. However, its role is highly context-dependent, with studies reporting both pro-migratory and inhibitory effects on gap closure. Here, we investigate the specific role of Piezo1 activation in a model of large epithelial gap closure using Madin-Darby Canine Kidney (MDCK) cells. We demonstrate that pharmacological activation of Piezo1 with Yoda1 significantly delays the closure of large gaps in a confluent monolayer. This delayed closure is not driven by changes in cell proliferation, pointing instead to a direct effect on the mechanics of collective cell migration. To elucidate the underlying molecular mechanism, we performed bulk RNA-sequencing on Yoda1-treated versus control MDCK cells. Transcriptomic analysis revealed that Piezo1 activation leads to significant differential expression of genes associated with integrin signaling, extracellular matrix (ECM) organization, and focal adhesions (FAs). These findings suggest that Yoda1-mediated Piezo1 activation impedes epithelial gap closure by modulating the transcriptional programs that govern cell-matrix adhesion and cytoskeletal dynamics, thereby disrupting the collective migration required to heal a large wound. This study provides new insights into the context-dependent inhibitory role of Piezo1 in epithelial repair and highlights the transcriptional axis through which it may operate.

ORGANISM(S): Canis lupus familiaris

PROVIDER: GSE324943 | GEO | 2026/03/18

REPOSITORIES: GEO

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