Abstract

Periostin plays an important role in the development of chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP). Glucocorticoids (GCs) are anti-inflammatory drugs used to treat CRS, but the mechanism for inhibiting periostin-induced tissue remodeling is still unclear. We sought to investigate the expression of periostin, α-SMA, and extracellular matrix (ECM) components in sinonasal tissues and to evaluate the inhibitory mechanism of GCs in nasal fibroblasts and mucosa. We measured the expression of periostin, α-SMA and ECM components in sinonasal tissues. Correlation of CRS severity and periostin was evaluated by the Lund-Mackey score. Fibroblasts and ex vivo culture of the inferior turbinate were used to investigate the effects of GCs on periostin-induced alterations using real-time PCR, western blot, and immunostaining. Wound healing, transwell invasion, and collagen gel contraction were performed to evaluate migration and collagen contraction. Periostin was highly expressed in eosinophilic CRSwNP and correlated with the Lund-Mackay score. In nasal fibroblasts, periostin increased tissue remodeling involved protein. GCs suppressed the alterations of periostin. In addition, periostin induced activation of Src/AKT/mTOR, which was inhibited by GCs. GCs also inhibited periostin-induced migration, invasion, and collagen gel contraction. We suggest that GCs are therapeutic agents for CRSwNP by inhibiting tissue remodeling through their inhibitory effect on Src/Akt/mTOR signaling pathway. This article is protected by copyright. All rights reserved.

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