Korean Circ J.
2001 Oct;31(10):1049-1058. 10.4070/kcj.2001.31.10.1049.
The Delayed Phase of Protection in Heat-Induced Preconditioning: Role of the Heat Shock Protein associated with cytoskeleton
- Affiliations
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- 1Department of Anatomy, College of Medicine, Kangwon National University, Chunchon, Korea.
- 2Department of Forensic medicine, National Institute of Scientific Investigation, Seoul, Korea.
- 3Department of Anatomical Pathology, College of Medicine, Donga University, Pusan.
- 4Department of Anatomy, School of Medicine, Sungkyunkwan University, Suwon, Korea.
- KMID: 2029592
- DOI: http://doi.org/10.4070/kcj.2001.31.10.1049
Abstract
- BACKGROUND AND OBJECTIVES
We investigated the ability of a brief heat shock on day one to provide delayed protection against lethal heat stress on day two in a rat-derived H9c2 cardiomyoblast cell line with reference to the role of heat shock protein 25/27, 70i and the p38MAPK signalling pathway. MATERIALS, METHODS AND RESULTS: Heat preconditioning(Heat P; 20min at 42+/-0.1degrees C) and adenosine(ADO) administered on day 1 protected against cell death under lethal heat challenge (75min at 42+/-0.1degrees C) on day 2 as measured by MTT test: ( % cell viability: Heat P: 79.9+/-3.23%, ADO: 71.9+/-4.10% vs. control: 52.7+/-1.65% respectively ). This protection was abolished by treatment with SB203580 or cytochalasine D prior to the protective stimulus on day 1( SB203580: 64.1+/-4.37%, cytochalasine D: 73.1+/-4.33% vs. Heat P ). Western blotting analysis indicated a significant accumulation of hsp70i in Heat P and SB203580-treated Heat P cells compared to control and adenosine-, SB203580-treated cells. Phosphorylation of hsp25 was significantly increased in Heat P cells compared to control cells. We also observed fragmentation of F-actin and formation of F-actin aggregates in cells exposed to lethal heat challenge. In contrast, the delayed cytoprotection preserved the F-actin bundles under lethal heat challenge. Hsp27-overexpressed, stable clones were more resistant to lethal heat shock when compared to control cells transfected with the vector alone.
CONCLUSION
These data suggest an important role for p38MAPK/hsp25/27 pathway as a potential distal effector of heat-induced delayed protection.
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