中華民國兒童胸腔醫學會論文摘要範本
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Chymase mediates paraquat-induced collagen expression in human lung fibroblasts
陳中明、汪棱芳、藍耀東
臺北醫學大學小兒科、生化科、醫學科學研究所 Chung-Ming Chen, Leng-Fang Wang, Yaw-Dong Lang
Department of Pediatrics, Biochemistry, and Graduate Institute of Medical Sciences, Taipei Medical University, Taipei, Taiwan
Survivors of paraquat poisoning may be left with pulmonary fibrosis and a restrictive type of pulmonary dysfunction. Angiotensin (Ang) II is an inducer of connective tissue growth factor (CTGF) expression in the heart and kidneys. Chymase converts Ang I to Ang II, which plays an important role in the pathogenesis of lung fibrosis. The aims of this study were to investigate the effects of paraquat on Ang II, CTGF, and collagen expressions and to assess the role of chymase and the mechanisms by which paraquat induces collagen expression in human lung fibroblasts. Human lung fibroblasts (MRC-5) were incubated with paraquat with or without the chymase inhibitor, chymostatin. Paraquat significantly increased angiotensinogen mRNA expression in a dose-dependent manner while angiotensin-converting enzyme (ACE) mRNA expressions were comparable at the paraquat concentrations of 0, 100, and 300 μM. Paraquat increased CTGF and collagen mRNA and protein expressions, chymase protein and chymase activities, and Ang II in a dose-dependent manner, and chymostatin inhibited these effects. The cDNA sequence of human lung fibroblasts is identical to that reported for human mast cells. In conclusion, the demonstration of a functional alternative pathway for Ang II generation by ACE and the fact that paraqaut-treated human lung fibroblasts are capable of producing and secreting chymase represent strong evidence of a physiological role for this enzyme in paraquat-induced lung fibrosis.
