ArticleExperimental and therapeutic medicine2016
Expression and location of HSP60 and HSP10 in the heart tissue of heat-stressed rats.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Heat Stress-Mediated Multi-Organ Injury: Pathophysiology and Treatment Strategies.Comprehensive Physiology · 2025Review
- The Emerging Role of Heat Shock Proteins in Nasopharyngeal Carcinoma: A Review.Current medicinal chemistry · 2025Review
- Chronic heat stress induces the expression ofFrontiers in genetics · 2023Article
- Deletion of heat shock protein 60 in adult mouse cardiomyocytes perturbs mitochondrial protein homeostasis and causes heart failure.Cell death and differentiation · 2020Article
- Fetal bovine serum inhibits neomycin-induced apoptosis of hair cell-like HEI-OC-1 cells by maintaining mitochondrial function.American journal of translational research · 2019Article
- Review
- Proteomic analysis of mitochondrial proteins in the guinea pig heart following long-term normobaric hyperoxia.Molecular and cellular biochemistry · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to analyze the expression levels and localizations of heat shock protein (HSP) 60 and HSP10 in the heart tissue of rats subjected to heat stress (42°C) for 0, 20, 80 and 100 min. Histopathological injuries and increased serum activities of serum lactate dehydrogenase and creatine kinase isoenzyme MB were detected in the heated rat myocardial cells. These results suggested that heat stress-induced acute degeneration may be sufficient to cause sudden death in animals by disrupting the function and permeability of the myocardial cell membrane. In addition, the expression levels of HSP60 were significantly increased following 20 min heat stress, whereas the expression levels of its cofactor HSP10 were not. Furthermore, the location of HSP60, but not of HSP10, was significantly altered during periods of heat stress. These results suggested that HSP60 in myocardial tissue may be more susceptive to the effects of heat stress as compared with HSP10, and that HSP10 is constitutively expressed in the heart of rats. The expression levels and localizations of HSP60 and HSP10 at the different time points of heat stress were not similar, which suggested that HSP60 and HSP10 may not form a complex in the heart tissue of heat-stressed rats.
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