tailieunhanh - Báo cáo khoa học: Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide attenuate the cigarette smoke extract-induced apoptotic death of rat alveolar L2 cells

Chronic obstructive pulmonary disease is a major clinical disorder usually associated with cigarette smoking. A central feature of chronic obstructive pulmonary disease is inflammation coexisting with an abnormal protease/anti-protease balance, leading to apoptosis and elastolysis. In anin vitro study of rat lung alveolar L2 cells, cigarette smoke extract (CSE) induced apoptotic cell death. Expo-sure of L2 cells to CSE at a concentration of resulted in a 50% increase of caspase-3 and matrix met-alloproteinase (MMP) activities. Specific inhibitors for caspases and MMPs attenuated the cytotoxicity of CSE. RT-PCR amplification identified VPAC2 receptors in L2 cells. . | Eur. J. Biochem. 271 1757-1767 2004 FEBS 2004 doi Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide attenuate the cigarette smoke extract-induced apoptotic death of rat alveolar L2 cells Satomi Onoue1 2 Yuki Ohmori3 Kosuke Endo1 Shizuo Yamada3 Ryohei Kimura3 and Takehiko Yajima2 1Health Science Division Itoham Foods Inc. Moriya Ibaraki Japan department of Analytical Chemistry Faculty of Pharmaceutical Sciences Toho University Funabashi Chiba Japan 3Department of Biopharmaceutical Sciences and COE Program in the 21st Century School of Pharmaceutical Sciences University of Shizuoka Shizuoka Japan Chronic obstructive pulmonary disease is a major clinical disorder usually associated with cigarette smoking. A central feature of chronic obstructive pulmonary disease is inflammation coexisting with an abnormal protease anti-protease balance leading to apoptosis and elastolysis. In an in vitro study of rat lung alveolar L2 cells cigarette smoke extract CSE induced apoptotic cell death. Exposure of L2 cells to CSE at a concentration of resulted in a 50 increase of caspase-3 and matrix metalloproteinase MMP activities. Specific inhibitors for caspases and MMPs attenuated the cytotoxicity of CSE. RT-PCR amplification identified VPAC2 receptors in L2 cells. A radioligand-binding assay with 125I-labeled vasoactive intestinal peptide VIP found high affinity and saturable 125I-labeled VIP-binding sites in L2 cells. VIP and pituitary adenylate cyclase-activating polypeptide PACAP27 were approximately equipotent for both VIP receptor binding and stimulation of cAMP production in L2 cells. Both neuropeptides at concentrations higher than 10 13 M produced a concentration-dependent inhibition of CSE-induced cell death in L2 cells. VIP at 10 7 M reduced CSE-stimulated MMP activity and caspase-3 activation. The present study has shown that VIP and PACAP27 significantly attenuate the cytotoxicity of CSE through the

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