The Delayed Phase of Protection in Heat-Induced Preconditioning: Role of the Heat Shock Protein associated with cytoskeleton.
10.4070/kcj.2001.31.10.1049
- Author:
Dae Joong KIM
1
;
Sang Yong LEE
;
Jeong Hyun PARK
;
Jang Hee HAHN
;
Sung Man PARK
;
Jin Sook JEONG
;
Ho Dirk KIM
Author Information
1. Department of Anatomy, College of Medicine, Kangwon National University, Chunchon, Korea.
- Publication Type:Original Article
- Keywords:
Preconditioning;
Heat shock protein;
Actin
- MeSH:
Actins;
Blotting, Western;
Cell Death;
Cell Line;
Cell Survival;
Clone Cells;
Cytoprotection;
Cytoskeleton*;
Heat-Shock Proteins*;
Hot Temperature*;
Phosphorylation;
Shock
- From:Korean Circulation Journal
2001;31(10):1049-1058
- CountryRepublic of Korea
- Language:Korean
-
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.
