Overexpression of the small heat shock protein, hsp27, confers resistance to hyperthermia, but not to oxidative stress and UV-induced cell death, in a stably transfected squamous cell carcinoma cell line.
Overexpression of the small heat shock protein, hsp27, confers resistance to hyperthermia, but not to oxidative stress and UV-induced cell death, in a stably transfected squamous cell carcinoma cell line.
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DOI：
10.1016/s1011-1344(96)00010-3
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发表时间：
1997-05
期刊：
影响因子：
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通讯作者：
F. Trautinger;C. Kokesch;I. Herbacek;R. Knobler;I. Kindås-mügge
中科院分区：
文献类型：
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作者：
F. Trautinger;C. Kokesch;I. Herbacek;R. Knobler;I. Kindås-mügge
27 kD热休克蛋白（hsp 27）表达在人角质形成细胞在体外和原位分化。本研究旨在探讨热休克蛋白27在角质形成细胞中的表达是否与热和紫外线辐射的有害影响的抵抗力增加有关。携带hsp 27的人基因的转染载体，在hsp 27以及SV 40启动子的控制下（pSG 2711，M. Jäättelä等人，11（1992）3507-3512）与新霉素抗性基因一起导入鳞状细胞癌细胞系A431。将细胞暴露于UVA、UVB、热（45 °C，4 h）或过氧化氢（0.025- 0.5mM），并测定存活细胞的百分比。热休克蛋白27的过度表达诱导增加抵抗高温，但不是过氧化氢介导的氧化损伤。当细胞暴露于增加量的UVA（5-80 J cm−2）和UVB（4-64 mJ cm−2）时，过表达hsp 27的克隆和对照克隆的存活细胞百分比相同。从这些数据中，我们得出结论，热休克蛋白27是一个介体的热耐受性，但不保护角质形成细胞从紫外线诱导的细胞死亡。
The 27 kD heat shock protein (hsp27) is expressed in human keratinocytes in association with differentiation in vitro and in situ. This study was conducted to investigate whether the expression of hsp27 in keratinocytes is associated with increased resistance to the deleterious effects of heat and UV radiation. A transfection vector carrying the human gene for hsp27, under the control of hsp27 as well as the SV40 promoter (pSG2711, M. Jäättelä et al., EMBO J. 11 (1992) 3507–3512), was introduced together with a neomycin-resistance gene into the squamous cell carcinoma cell line A431. Cells were exposed to either UVA, UVB, heat (45 °C, 4 h) or hydrogen peroxide (0.025-0.5 mM) and the percentage of surviving cells was determined. Overexpression of hsp27 induced increased resistance to hyperthermia, but not to hydrogen peroxide-mediated oxidative injury. When cells were exposed to increasing amounts of UVA (5–80 J cm−2) and UVB (4–64 mJ cm−2), the percentage of surviving cells was identical for clones overexpressing hsp27 and control clones. From these data, we conclude that hsp27 is a mediator of thermotolerance, but does not protect keratinocytes from UV-induced cell death.