Anoctamin-1 is induced by TGF-beta and contributes to lung myofibroblast differentiation.

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by progressive scarring of the lungs and resulting in deterioration in lung function. Transforming growth factor-beta (TGF-β) is one of the most established drivers of fibrotic processes. TGF-β promotes transformation of tissue fibroblasts to myofibroblasts, a key finding in the pathogenesis of pulmonary fibrosis. We report here that TGF-β robustly upregulates the expression of the calcium-activated chloride channel Anoctamin-1 (ANO1) in human lung fibroblasts (HLF) at mRNA and protein levels. ANO1 is readily detected in fibrotic areas of IPF lungs in the same area with smooth muscle alpha-actin (SMA)-positive myofibroblasts. TGF-β-induced myofibroblast differentiation (determined by the expression of SMA, collagen-

SUBMITTER: Reed EB 

PROVIDER: S-EPMC10274757 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature