Howard G, Geoghegan T E
Mol Cell Biochem. 1986 Feb;69(2):155-60. doi: 10.1007/BF00224762.
Anoxia has been shown to induce the expression of one or more "stress proteins' in mammalian cells and tissues. A less severe form of oxygen depletion, hypoxic hypoxia, occurs in response to hypobaric decompression which simulates high altitude conditions. Under these conditions mouse hearts accumulate mRNAs for at least two polypeptides at substantially elevated levels. The molecular weights of these proteins, 85 kDa and 95 kDa, are similar to those reported for other mammalian stress proteins or glucose-regulated proteins. Time course experiments suggest that mRNAs for these species increase continuously for up to 16 hours of treatment, while mRNA for 71 kDa and 79 kDa polypeptides are elevated early in the treatment, but later decrease to control values. Total heart mRNA template activity is also increased by the hypobaric treatment. These results demonstrate that mouse cardiac tissue is capable of mounting a cellular stress-like response when exposed to moderately stressful conditions. It also provides a model for studying the direct effects of acute hypoxic stress on cellular gene expression, and its relationship to physiological adaptation.
缺氧已被证明可诱导哺乳动物细胞和组织中一种或多种“应激蛋白”的表达。一种不太严重的氧耗竭形式,即低氧性缺氧,是对模拟高海拔条件的低压减压的反应。在这些条件下,小鼠心脏中至少两种多肽的mRNA大量积累且水平显著升高。这些蛋白质的分子量分别为85 kDa和95 kDa,与其他哺乳动物应激蛋白或葡萄糖调节蛋白的分子量相似。时间进程实验表明,在长达16小时的处理过程中,这些种类的mRNA持续增加,而71 kDa和79 kDa多肽的mRNA在处理早期升高,但随后降至对照值。低压处理也会增加心脏总mRNA模板活性。这些结果表明,小鼠心脏组织在暴露于适度应激条件下时能够产生类似细胞应激的反应。它还为研究急性低氧应激对细胞基因表达的直接影响及其与生理适应的关系提供了一个模型。