Bush asks for 13 per cent extra for science.
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Biomedical subjects
Publications and source records attributed to D Gershon.
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An age-related impairment in the induction of heat-shock proteins (HSPs), which are thought to comprise a protective or adaptive response to cellular stress, may contribute to a reduction in thermal tolerance with age. When 5- and 24-mo-old rats were exposed to ambient temperatures of 23, 35, 37.5, or 40 degrees C for 90 min, a graded increase in the level of HSP70 mRNA expression was observed in brain, lung, and skin of animals from both groups. However, at temperatures above 23 degrees C, HSP70 expression was less in tissues of older rats when compared with those of young animals. This relative decline of heat-induced HSP70 mRNA levels with age correlated with an attenuated increase in colonic temperature (Tc) of old rats resulting from heat exposure. In other experiments, it was determined that the duration of hyperthermia was also an important factor in determining the level of HSP70 mRNA expression in vivo. Thus age-related differences in heat-induced HSP70 mRNA expression appear to result from differences in Tc due to heat stress rather than an impairment in the regulation of HSP70 gene expression.
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Although the induction of heat shock proteins (HSP) has been studied extensively in cultured cells, comparatively few studies have examined their expression in vivo. In this report, mRNA expression of two HSP families, HSP70 and HSP27, was investigated in brain, liver, lung, and skin of rats exposed to elevated ambient temperatures. The time course and relative magnitude of the heat-induced expression for these two HSP differed between tissues of the same animal. Even within the same tissue, HSP70 and HSP27 displayed differential kinetics of induction. In brain, lung, and skin, induction of HSP70 was dependent on the duration and temperature of the heat stress. This induction was transient with maximal HSP70 expression occurring at 1 h and returning to baseline 3 h after removal of the animals from heat stress. In liver, HSP70 expression did not show a direct relationship with temperature conditions and maximal induction did not occur until 6 h after heat stress. Heat-induced HSP27 expression was dependent on time and temperature of exposure in lung and skin but not in brain and liver. These findings demonstrate that the heat shock response in vivo lacks much of the coordinate control of expression characteristic of cultured cell populations and suggest that mechanisms controlling this cellular stress response are influenced by physiologic factors that cannot be studied in vitro.
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