Experimental Fluid Percussion Brain Injury Induces Temporally and Regionally Specific Expressions of Heat Shock Protein Genes.
- Author:
Younghwa KIM
1
;
Dal Soo KIM
;
Sun Hwa PARK
;
Tae Sik KIM
;
Woong SUN
;
Hyun KIM
;
Changmee KIM
Author Information
1. Department of Anatomy, College of Medicine, Brain Korea 21, Korea University, Seoul, Korea. cmkim@korea.ac.kr
- Publication Type:Original Article
- Keywords:
FP-brain injury;
Hsp genes;
Apoptosis;
In situ hybridization
- MeSH:
Adult;
Animals;
Apoptosis;
Brain Injuries*;
Brain*;
Heat-Shock Proteins*;
Hot Temperature*;
Humans;
In Situ Hybridization;
Percussion*;
Rats;
Shock
- From:Korean Journal of Anatomy
2004;37(1):43-50
- CountryRepublic of Korea
- Language:English
-
Abstract:
Although the induction of various members of hsp (heat shock protein) gene family has been linked to the resistance to apoptosis by a range of diverse stress stimuli, detail information has not been available yet as to the temporal and spatial expression patterns of various hsp genes after traumatic brain injury. In the present study, using a lateral fluid percussion (FP) injury as a model of traumatic brain injury, expression profiles of stress induced hsp genes were comparatively evaluated in the adult rat brain by in situ hybridization (ISH). We found that the temporal and regional expression patterns between the hsp70 superfamily members, hsp110 and hsp70, and the small hsp member, hsp25 are distinct. While the hsp110 and hsp70 expression was observed as early as 1 hr after injury and maximally induced at 3 hr after injury, the hsp25 expression appeared 6 hr after injury and the expression sustained until 6 days after the injury. Moreover, the expression of hsp110 and hsp70 was localized primarily in the impact site, that of the small hsp25 was observed throughout the ipsilateral cortical area in the distant regions remote from the impact site as well as in the impact site following injury. These results suggest that the sequential and combinatorial manipulation of various hsp genes can be exploited in reducing acute and delayed post-traumatic apoptosis and associated neurological dysfunction.
