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The objective of this study is to investigate the role of antisense oligodeoxynucleotide (ASODN) of basic fibroblast growth factor (bFGF) in the proliferation, differentiation and collagen synthesis of pulmonary fibroblasts (PFs) and the possible mechanism. PFs were isolated from male Wistar Rat and transfected with antisense oligodeoxynucleotide or sense oligodeoxynucleotide (SODN) of bFGF for four experimental conditions: (1) control group: PFs without TGF-β1; (2) TGF-β1 group: PFs with TGF-β1; (3) TGF-β1+ASODN group: ASODN transfected PFs with TGF-β1; and (4) TGF-β1+SODN group: SODN transfected PFs with TGF-β1. Proliferation of PFs was monitored by growth curves and MTT assays, expression of α-smooth muscle actin (α-SMA) was evaluated by immunocytochemistry, concentrations of bFGF, CTGF, and Type I collagen in culture supernatants were determined by ELISA, and mRNA expression of Smad3, Smad7 and Type I collagen in pulmonary fibroblasts was detected by RT-PCR. We found that SODN of bFGF increased cell proliferation of PFs, enhanced the expression level of bFGF, CTGF, α-SMA, type I collagen and Smad3. However, ASODN of bFGF had the opposite effects. However, Smad7 was increased in TGF-β1+SODN group but decreased in TGF-β1+ASODN group. The proliferation, differentiation, and collagen synthesis of PFs could be promoted by bFGF and inhibited by ASODN of bFGF which may be related to the regulation of TGF-β1-Smad signaling pathway.

cytologia

TGF-β1-Induced Pulmonary Fibroblasts Proliferation and Differentiation Are Inhibited by Antisense Oligodeoxynucleotide of Basic Fibroblast Growth Factor