Shuling Hao1, Weiping Wang2, Zhonghe Yu3, Jiandong Li1. 1. Department of Respiratory Disease, Military General Hospital of Beijing PLA, Beijing 100700, China. 2. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University, Beijing 100191, China. 3. Department of Oncology Disease, Military General Hospital of Beijing PLA, Beijing 100700, China.
Abstract
OBJECTIVE: To observe the effects of adrenomedullin (AM) on transforming growth factor- β1 (TGF-β1) induced the expression of procollagen type 1 alpha 1 (Col1α1) and procollagen type 3 alpha 1 (Col3α1) as well as Smad2/3 phosphorylation in human fetal lung fibroblasts (HFLFs). METHODS: Primary HFLFs were cultured in vitro. After treated with TGF-β1 and/or AM, the expression levels of Col1α1 and Col3α1 mRNA were determined by reverse transcription PCR (RT-PCR), and phospho-Smad2/3 (p-Smad2/3) protein levels in HFLFs were measured by Western blotting. RESULTS: TGF-β1 increased the gene expression levels of Col1α1 and Col3α1, and promoted the phosphorylation levels of Smad2/3 protein in HFLFs. AM significantly reversed the expression level of Col3α1 mRNA, and inhibited p-Smad2/3 expression in HFLFs induced by TGF-β1. CONCLUSION: AM could inhibit TGF-β1-induced the procollagen expression in cultured HFLFs possibly through the Smad2/3 signaling pathway.
OBJECTIVE: To observe the effects of adrenomedullin (AM) on transforming growth factor- β1 (TGF-β1) induced the expression of procollagen type 1 alpha 1 (Col1α1) and procollagen type 3 alpha 1 (Col3α1) as well as Smad2/3 phosphorylation in human fetal lung fibroblasts (HFLFs). METHODS: Primary HFLFs were cultured in vitro. After treated with TGF-β1 and/or AM, the expression levels of Col1α1 and Col3α1 mRNA were determined by reverse transcription PCR (RT-PCR), and phospho-Smad2/3 (p-Smad2/3) protein levels in HFLFs were measured by Western blotting. RESULTS: TGF-β1 increased the gene expression levels of Col1α1 and Col3α1, and promoted the phosphorylation levels of Smad2/3 protein in HFLFs. AM significantly reversed the expression level of Col3α1 mRNA, and inhibited p-Smad2/3 expression in HFLFs induced by TGF-β1. CONCLUSION: AM could inhibit TGF-β1-induced the procollagen expression in cultured HFLFs possibly through the Smad2/3 signaling pathway.