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细胞对紫外线辐射反应中的应激蛋白。

Stress proteins in the cellular response to ultraviolet radiation.

作者信息

Trautinger F, Kindås-Mügge I, Knobler R M, Hönigsmann H

机构信息

Department of Dermatology, University of Vienna, Austria.

出版信息

J Photochem Photobiol B. 1996 Sep;35(3):141-8. doi: 10.1016/s1011-1344(96)07344-7.

DOI:10.1016/s1011-1344(96)07344-7
PMID:8933720
Abstract

Virtually all cells-from prokaryotes to highly differentiated mammalian tissues-respond to a sudden increase in temperature with increased production of a limited set of proteins, called heat shock proteins or stress proteins (hsp). Other stress factors such as alcohol, heavy metals, oxidants and agents leading to protein denaturation are equally able to induce a similar response. Induction of hsp is followed by a transient state of increased resistance to further stress. Many hsp function as "molecular chaperones" by binding to partially folded or misfolded proteins thus preventing their irreversible denaturation during stress exposure. The high evolutionary conservation of this reaction suggests its importance for the survival of cells and tissues under hostile environment conditions. Ultraviolet radiation (UV) exerts many potentially harmful effects on prokaryotic and eukaryotic cells and hsp may help the cell to cope with UV-induced damage. This review will focus on the role of hsp in the cellular response of mammalian skin to UV. Hsp have been detected in resting as well as stress exposed epidermal and dermal cells and experimental evidence points to the fact that these proteins mediate protection from UV induced cell death in vitro and in vivo. Experimental studies further indicate that UV itself might be able to induce the expression of specific hsp. Thus, hsp might provide an adaptive cellular response to increasing exposure to UV. Furthermore, UV-activation of hsp synthesis may provide a valuable model for investigation of the transcription regulation of UV-induced gene expression.

摘要

实际上,所有细胞——从原核生物到高度分化的哺乳动物组织——都会对温度突然升高做出反应,产生一组有限的蛋白质,即热休克蛋白或应激蛋白(hsp),其产量会增加。其他应激因素,如酒精、重金属、氧化剂以及导致蛋白质变性的物质,同样能够诱导类似的反应。hsp的诱导之后会出现对进一步应激的抗性增加的短暂状态。许多hsp通过与部分折叠或错误折叠的蛋白质结合而发挥“分子伴侣”的作用,从而在应激暴露期间防止其不可逆变性。这种反应在进化上的高度保守性表明其对于细胞和组织在恶劣环境条件下生存的重要性。紫外线辐射(UV)对原核细胞和真核细胞会产生许多潜在的有害影响,而hsp可能有助于细胞应对紫外线诱导的损伤。本综述将聚焦于hsp在哺乳动物皮肤对紫外线的细胞反应中的作用。在静息以及应激暴露的表皮和真皮细胞中均检测到了hsp,实验证据表明这些蛋白质在体外和体内介导了对紫外线诱导的细胞死亡的保护作用。实验研究进一步表明,紫外线本身可能能够诱导特定hsp的表达。因此,hsp可能为增加紫外线暴露提供一种适应性细胞反应。此外,hsp合成的紫外线激活可能为研究紫外线诱导的基因表达的转录调控提供一个有价值的模型。

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