Hsp-72, a candidate prognostic indicator of heatstroke |
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Authors: | Mohammed Dehbi Engin Baturcam Abdelmoneim Eldali Maqbool Ahmed Aaron Kwaasi Muhammad Azhar Chishti Abderrezak Bouchama |
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Institution: | (1) Department of Comparative Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, 11211, Saudi Arabia;(2) Institute of Musculoskeletal Sciences, University of Oxford, Oxford, UK;(3) Department of Biochemistry & Obesity Research Centre, College of Medicine, King Saud University, Riyadh, 11461, Saudi Arabia;(4) Department of Adult Critical Care Medicine, King Faisal Specialist Hospital and Research Centre, Riyadh, 11211, Saudi Arabia;(5) Present address: Dasman Institute for Research, Education & Prevention of Diabetes and Other Chronic Diseases, P.O. Box 1180, Dasman, 15462 Kuwait, Kuwait |
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Abstract: | 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°C (moderate heatstroke) or occurrence of hypotension
associated with core temperature ≥43.5°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. |
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Keywords: | Heat stress Heatstroke Baboon Heat shock proteins Hyperthermia Multiple organ dysfunction syndrome |
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