Li G C, Werb Z
Proc Natl Acad Sci U S A. 1982 May;79(10):3218-22. doi: 10.1073/pnas.79.10.3218.
Synthesis of a family of proteins called "heat shock" proteins is induced or enhanced in cells in response to various environmental stresses, suggesting that these proteins may perform functions essential to cell survival. Because a brief, nonlethal heat treatment can dramatically induce a transient resistance to a subsequent lethal heat treatment (thermotolerance), we examined the effect of heat treatment (41-46 degrees C) on protein synthesis and cell survival in plateau-phase Chinese hamster fibroblast (HA-1) cells. After heat treatments that either drastically inhibited total protein synthesis (46 degrees C) or did not suppress it (41 degrees C), the synthesis of heat shock proteins was greatly enhanced over that in unheated cells, and cell survival was increased 10(2)- to 10(6)-fold when cells were challenged by a subsequent lethal heat treatment. The synthesis of heat shock proteins correlated well with the development of thermotolerance, and the stability of these proteins correlated well with the persistence of thermotolerance up to 36 hr. Sodium arsenite, hypoxia, and ethanol also induced both the synthesis of heat shock proteins and transient thermotolerance. A qualitative analysis of individual proteins suggests that the synthesis and persistence of polypeptides of Mr 70,000 or 87,000 most closely conformed to the kinetics of thermotolerance.
在细胞中，响应各种环境应激会诱导或增强一类名为“热休克”蛋白的蛋白质的合成，这表明这些蛋白质可能执行对细胞存活至关重要的功能。由于短暂的、非致死性的热处理可显著诱导对随后致死性热处理的短暂抗性（热耐受性），我们研究了热处理（41 - 46摄氏度）对处于平台期的中国仓鼠成纤维细胞（HA - 1）中蛋白质合成和细胞存活的影响。在进行了大幅抑制总蛋白质合成的热处理（46摄氏度）或未抑制总蛋白质合成的热处理（41摄氏度）后，热休克蛋白的合成比未加热的细胞大大增强，并且当细胞受到随后的致死性热处理挑战时，细胞存活率提高了10²至10⁶倍。热休克蛋白的合成与热耐受性的发展密切相关，并且这些蛋白质的稳定性与热耐受性持续长达36小时密切相关。亚砷酸钠、缺氧和乙醇也诱导热休克蛋白的合成以及短暂的热耐受性。对单个蛋白质的定性分析表明，分子量为70,000或87,000的多肽的合成和持久性与热耐受性的动力学最为吻合。
