The extracellular matrix protein periostin is required for wound repair in primary human airway epithelia

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Article: The extracellular matrix protein periostin is required for wound repair in primary human airway epithelia

Authors: Lorena A Tran, Michael Catlin, Scott Schecter, Andrew L Thurman, Shreya Ghimire, Rosarie A Tudas, Brandon Bettis, Ryan M Gannon, Joseph Zabner, Alejandro A Pezzulo

Journal: Am J Physiol Lung Cell Mol Physiol. 2025 Jun 1;328(6):L826-L831

Abstract:
Type 2 inflammation and epithelial-to-mesenchymal transitions (EMTs) play critical roles in airway repair after damage from allergens or parasites. The matricellular protein periostin (POSTN) has increased expression in inflammatory conditions and has been implicated in fibrosis and EMT, suggesting a role in airway repair. This study investigates the role of periostin in airway epithelial and lung fibroblast wound repair using an in vitro wound model. Our results demonstrate that the type 2 cytokine IL-13 induces periostin secretion from primary human airway epithelial basal cells. Periostin knockdown in human airway epithelial cells (HAEs) and human lung fibroblasts (HLFs) impairs wound closure, indicating that periostin is required for airway repair. In a coculture model of HAE and HLFs, fibroblast-secreted POSTN is required for airway epithelial wound repair, suggesting that periostin is involved in paracrine signaling between the two cell types. These findings highlight periostin’s critical function in epithelial and fibroblast-mediated wound repair, suggesting its potential as a therapeutic target for diseases characterized by aberrant wound healing and fibrosis, such as asthma and idiopathic pulmonary fibrosis. NEW & NOTEWORTHY: This article highlights the critical role of periostin (POSTN) in airway epithelial and fibroblast-mediated wound repair. Moreover, the study reveals a paracrine signaling loop between airway epithelial basal cells and lung fibroblasts, emphasizing periostin’s therapeutic potential for diseases like asthma and idiopathic pulmonary fibrosis.

Link to journal online: https://journals.physiology.org/doi/full/10.1152/ajplung.00039.2025

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