Department of Comparative Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia.
Cell Stress Chaperones. 2010 Sep;15(5):593-603. doi: 10.1007/s12192-010-0172-3. Epub 2010 Feb 23.
Exposure of rats to environmental heat enhances the expression of heat shock protein-72 (Hsp-72) in most of their organs proportionally to heat stress severity. Pre-induction or over-expression of Hsp-72 prevents organ damage and lethality, suggesting that heat shock proteins (Hsps) may have a pathogenic role in this condition. We investigated the expression profile of Hsps in baboons subjected to environmental heat stress until the core temperature attained 42.5 degrees C (moderate heatstroke) or occurrence of hypotension associated with core temperature > or = 43.5 degrees C (severe heatstroke). Western blot analysis demonstrated a differential induction of Hsp-72 among organs of heat-stressed animals with the highest induction in the liver and the lowest in lung. Hsp-60 and Hsc-70 expression was similar between control and heat-stressed animals. ELISA studies indicated a marked release of Hsp-72 into the circulation of baboons with severe heatstroke with a peak at 24 h post-heatstroke onset and remained sustained up to 72 h. Hsp-72 release was not associated with core temperature or systolic blood pressure, but correlated with markers of liver, myocardium, and skeletal muscle tissue necrosis. Non-survivors displayed significantly higher Hsp-72 levels than survivors. No Hsp-60 was detected in the circulation. These findings add further evidence that increased expression of Hsp-72 may be an important component of the host response to severe heatstroke. They also suggest that extracellular Hsp-72 is a marker of multiple organs tissue damage. Whether extracellular Hsp-72 plays a role in the host immune response to heat stress merits further studies.
暴露于环境热中会增强大鼠大多数器官中热休克蛋白-72（Hsp-72）的表达，其比例与热应激的严重程度成正比。Hsp-72 的预先诱导或过表达可防止器官损伤和致死，这表明热休克蛋白（Hsps）可能在这种情况下具有发病作用。我们研究了暴露于环境热应激下的狒狒的 Hsps 表达谱，直到核心温度达到 42.5 摄氏度（中度中暑）或出现与核心温度≥43.5 摄氏度相关的低血压（重度中暑）。Western blot 分析表明，热应激动物器官中 Hsp-72 的诱导存在差异，肝脏中的诱导最高，而肺中的诱导最低。Hsp-60 和 Hsc-70 的表达在对照和热应激动物之间相似。ELISA 研究表明，严重中暑的狒狒中有明显的 Hsp-72 释放到循环中，在中暑后 24 小时达到峰值，并持续至 72 小时。Hsp-72 的释放与核心温度或收缩压无关，但与肝、心肌和骨骼肌组织坏死的标志物相关。非幸存者的 Hsp-72 水平明显高于幸存者。循环中未检测到 Hsp-60。这些发现进一步证明，Hsp-72 的表达增加可能是宿主对严重中暑反应的重要组成部分。它们还表明，细胞外 Hsp-72 是多个器官组织损伤的标志物。细胞外 Hsp-72 是否在宿主对热应激的免疫反应中发挥作用值得进一步研究。
