Apolipoprotein A1 Inhibits TGF-β1-Induced Epithelial-to-Mesenchymal Transition of Alveolar Epithelial Cells

Baek, Ae Rin; Lee, Ji Min; Seo, Hyun Jung; Park, Jong Sook; Lee, June Hyuk; Park, Sung Woo; Jang, An Soo; Kim, Do Jin; Koh, Eun Suk; Uh, Soo Taek; Kim, Yong Hoon; Park, Choon Sik

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자료유형: 학술저널

저자정보: Baek, Ae Rin (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Lee, Ji Min (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Seo, Hyun Jung (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Park, Jong Sook (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Lee, June Hyuk (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Park, Sung Woo (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Jang, An Soo (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Kim, Do Jin (Division of Allergy and Respiratory Medicine, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital) Koh, Eun Suk (Department of Pa) Uh, Soo Taek Kim, Yong Hoon Park, Choon Sik

저널정보: 대한결핵 및 호흡기학회 Tuberculosis and Respiratory Diseases 결핵 및 호흡기 질환 제79권 제3호

발행연도: 2016.1

수록면: 143 - 152 (10page)

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Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor ${\beta}1$ (TGF-${\beta}1$)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-${\beta}1$-induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-${\beta}1$ with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and ${\alpha}$-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-${\beta}1$ receptor type 1 ($T{\beta}RI$) and type 2 ($T{\beta}RII$) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-${\beta}1$-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-${\beta}1$-induced change of the EMT phenotype. ApoA1 inhibited the TGF-${\beta}1$-induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-${\beta}1$-induced increase in $T{\beta}RI$ and $T{\beta}RII$ expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-${\beta}1$-induced EMT in experimental lung fibrosis.

#Apolipoprotein A-1 #Transforming Growth Factor Beta1 #Epithelial-Mesenchymal Transition #Pulmonary Fibrosis

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이 논문의 저자 정보

Baek, Ae Rin

소속기관 Division of Respiratory and Allergy, Department of Internal Medicine, Soonchunhyang University Buche

주요연구분야 의약학 > 임상의학 > 내과학

논문수 3 이용수 10

Lee, Ji Min