Simvastatin Attenuates TGF-�1-Induced Epithelial-Mesenchymal Transition in Human Alveolar Epithelial Cells | Zendy

Tuo Yang | Zendy; Miaomiao Chen | Zendy; Tieying Sun | Zendy

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Simvastatin Attenuates TGF-�1-Induced Epithelial-Mesenchymal Transition in Human Alveolar Epithelial Cells

Author(s) -

Tuo Yang,

Miaomiao Chen,

Tieying Sun

Publication year - 2013

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000350104

Subject(s) - vimentin , ctgf , epithelial–mesenchymal transition , fibronectin , a549 cell , mesenchymal stem cell , transforming growth factor , blot , cell migration , cell culture , chemistry , biology , transforming growth factor beta , fibrosis , connective tissue , microbiology and biotechnology , cancer research , growth factor , medicine , extracellular matrix , immunology , downregulation and upregulation , immunohistochemistry , receptor , biochemistry , genetics , gene

Transforming growth factor-β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AEC) may contribute to idiopathic pulmonary fibrosis (IPF). TGF-β1-induced EMT in A549 cells (a human AEC cell line) resulted in the adoption of mesenchymal responses that were predominantly mediated via the TGF-β1-Smad2/3 signaling pathway. Simvastatin (Sim), a 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase inhibitor, has been previously reported to inhibit EMT in human proximal tubular epithelial cells and porcine lens epithelial cells and to suppress Smad2/3 phosphorylation in animal models. However, whether Sim can attenuate TGF-β1-induced EMT in A549 cells and its underlying mechanisms remains unknown.

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