Induction of translational thermotolerance in liver of thermally stressed rats.

Induction of translational thermotolerance in liver of thermally stressed rats.
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热应激大鼠肝脏平移耐热性的诱导。

DOI:
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发表时间:
1993
期刊:
European Journal of Biochemistry
影响因子:
--
通讯作者:
T. Buchman
T. Buchman
中科院分区:
--
文献类型:
--
作者:
A. Maio;S. C. Beck;T. Buchman

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热休克基因在单细胞类型的培养物中的表达已被很好地描述,但对体内完整器官的热休克反应知之甚少。本研究对大鼠肝脏热休克基因表达的动力学和耐热性的诱导进行了研究。通过将核心体温提高到41摄氏度或42摄氏度,30分钟,动物受到确定的可逆应激。热休克-70蛋白家族的诱导形式(HSP-72)的新合成在两种温度下同时达到峰值和HSP-72转录本的最高水平。这些数据与先前在热应激后肝母细胞瘤细胞培养中观察到的结果一致[De Maio,A.,Beck,S.C.&Buchman,T.G.(1993)Circ.冲击40,177-186]。在42℃热休克后的第一个小时内,肝脏对多肽的放射性氨基酸的掺入被阻断。这种由热应激引起的蛋白质合成抑制可以通过在42℃预应激30分钟并允许大鼠在正常体温(37℃)下恢复24小时来防止。这种现象以前被定义为翻译耐热性,与肝脏中HSP-72的含量有关;最大保护发生在42℃热应激后24小时,此时HSP-72(蛋白质)也达到最大值,并随着HSP-72从肝脏中清除而减少。这些数据表明,肝脏中HSP-72的存在可能调节器官对随后应激的反应,并可能对反复侮辱后的器官和动物的生存起重要作用。
Heat-shock gene expression in cultures of single cell types has been well characterized but little is known about the heat-shock response of intact organs in vivo. In this study, the kinetics of hepatic heat-shock gene expression and the induction of thermotolerance were characterized in rats. Animals were subjected to a defined, reversible stress by increasing the core body temperature to 41 degrees C or 42 degrees C for 30 min. New synthesis of the inducible form of the heat shock-70 family of proteins (hsp-72) peaked simultaneously with the maximal level of hsp-72 transcripts at both temperatures. These data are consistent with previous observations in cultures of hepatoblastoma cells after thermal stress [De Maio, A., Beck, S. C. & Buchman, T. G. (1993) Circ. Shock 40, 177-186]. The incorporation of radioactive amino acids into polypeptides by the liver was blocked during the first hour of recovery after heat shock at 42 degrees C. This inhibition of protein synthesis by thermal stress could be prevented by prestressing rats at 42 degrees C for 30 min and allowing the rats to recover for 24 h at normal body temperature (37 degrees C). This phenomenon, previously defined as 'translational thermotolerance', correlates with the hepatic content of hsp-72; maximal protection occurs 24 h after a 42 degrees C thermal stress when hsp-72 (protein) is also maximum and decreases with the clearance of hsp-72 from the liver. These data suggest that the presence of hsp-72 within the liver may modulate the organ response to subsequent stresses and may be important to organ and animal survival after repeated insults.
DOI: --
发表时间: 1990
期刊: Surgery
影响因子: 3.8
作者:
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发表时间: 1985
影响因子: 5.3
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发表时间: 1991-04-01
影响因子: --
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DOI: --
发表时间: 1990
期刊: The Journal of biological chemistry
影响因子: --
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