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人支气管上皮细胞系中一种45 kD蛋白的协同表达与臭氧毒性

Coordinated expression of a 45 kD protein and ozone toxicity in a human bronchial epithelial cell line.

作者信息

Sun W, Wu R, Last J A

机构信息

California Regional Primate Research Center, Davis 95616-8542.

出版信息

Am J Respir Cell Mol Biol. 1994 Jun;10(6):673-82. doi: 10.1165/ajrcmb.10.6.7516174.

Abstract

The human bronchial epithelial cell line, BEAS-2B, which was immortalized by transformation with SV40 virus, when grown biphasically between 0.1 and 1.0 ppm of ozone and liquid medium showed increased release of Cr, decreased synthesis of various macromolecules, and decreased cell viability. Cell injury was a function of the concentration of ozone to which the cells were exposed. Furthermore, in proportion to the extent of cell injury, ozone exposure also induced and/or enhanced synthesis of a 45 kD protein but not any of the well-characterized heat shock proteins, e.g., HSP 70. Actinomycin D prevented enhanced synthesis of the 45 kD protein in cells exposed to ozone, suggesting transcriptional regulation of expression of the 45 kD protein. Enhanced synthesis of the 45 kD protein was not observed in cells treated with heat, cigarette smoke condensate, hydrogen peroxide, or bleomycin. High concentrations of glutathione added to the culture medium reduced ozone toxicity and ozone-enhanced synthesis of the 45 kD protein. These results suggest that ozone injury and enhanced expression of a gene encoding a 45 kD protein of as yet unknown function are coordinated in the SV40-immortalized bronchial epithelial cells.

摘要

人支气管上皮细胞系BEAS - 2B由SV40病毒转化永生化,当在0.1至1.0 ppm臭氧与液体培养基中双相生长时,显示铬释放增加、各种大分子合成减少以及细胞活力下降。细胞损伤是细胞暴露于臭氧浓度的函数。此外,与细胞损伤程度成比例,臭氧暴露还诱导和/或增强了一种45 kD蛋白的合成,但未诱导和/或增强任何已充分表征的热休克蛋白,例如HSP 70。放线菌素D可阻止暴露于臭氧的细胞中45 kD蛋白的合成增强,提示45 kD蛋白表达受转录调控。在用热、香烟烟雾冷凝物、过氧化氢或博来霉素处理的细胞中未观察到45 kD蛋白合成增强。向培养基中添加高浓度谷胱甘肽可降低臭氧毒性以及臭氧增强的45 kD蛋白合成。这些结果表明,在SV40永生化支气管上皮细胞中,臭氧损伤与编码功能未知的45 kD蛋白的基因表达增强是协同发生的。

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