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作 者:白洪波[1,2] 刘永平[3] 段佳熙[1] 周勇[1] 孙国瑛[1] 管茶香[1]
机构地区:[1]中南大学湘雅医学院生理学系,长沙410008 [2]广州医学院生理学教研室,广州510182 [3]湖南中医药大学生理学教研室,长沙410208
出 处:《中国应用生理学杂志》2012年第4期346-349,共4页Chinese Journal of Applied Physiology
基 金:国家自然科学基金资助项目(30870915);湖南省高校创新平台开放基金资助项目(11K077)
摘 要:目的:探讨降钙素基因相关肽(CGRP)对臭氧(O3)应激后人支气管上皮细胞(HBECs)中E-钙粘素(E-cd)表达的影响及机制。方法:采用RT-PCR检测E-cd mRNA的表达,免疫细胞化学染色法检测E-cd蛋白的表达。结果:CGRP呈剂量依赖性增加正常以及O3应激后HBECs胞膜上E-cd的表达,而对胞浆内E-cd的表达无明显影响;CGRP对HBECs胞膜上E-cd表达的上调作用可分别被H-89(PKA抑制剂)、H-7(PKC抑制剂)及W-7(CaM抑制剂)部分逆转。结论:CGRP可剂量依赖性增加正常和O3应激后HBECs胞膜E-cd的表达,而对胞浆内E-cd的表达无影响。Objective: To discuss the effect of calcitonin gene-related peptides (CGRP) on epithelial cadherin (E-cd) expression in human bronchial epithelial cells(HBECs) in vitro. Methods: The effect of CGRP on E-cd protein and mRNA expression in both normal and O3- challenged HBECs were determined by immunocytochemistry and RT-PCR. The signal transducfion pathways of CGRP were observed by using protein kinase C(PKC) inhibitor (H-7), calmodulin(CaM) inhibitor (W-7) and PKA inhibitor (H-89). Results: CGRP increased E-cd mRNA and protein expressions of normal and O3-challenged HBECs in a dose-dependent manner. CGRP had no effect on cytoplasm E-cd expression. Pre-treatment with H-89, H-7 and W-7, the up-regulatory effect of CGRP on E-cd expression was partly abolished. Conclusion: CGRP increased in cytomembrane E-cd expression of normal and O3-challenged HBECs in a dose-dependent manner. E-cd expression on HBECs was strengthened by CGRP via PKA, PKC and CaM pathways.
关 键 词:降钙素基因相关肽 E-钙粘素 支气管上皮细胞 臭氧
分 类 号:R332[医药卫生—人体生理学]
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