Keywords :
Animals; Carrier Proteins/biosynthesis; Coronary Vessels; Creatine Kinase/blood; DNA-Binding Proteins/biosynthesis; Early Growth Response Protein 1; Genes, Immediate-Early; Genes, fos; Genes, jun; HSC70 Heat-Shock Proteins; HSP70 Heat-Shock Proteins/biosynthesis; Heart/physiology/physiopathology; Heat-Shock Proteins/biosynthesis; Hot Temperature; Immediate-Early Proteins; In Situ Hybridization; Kinetics; Male; Myocardial Contraction; Myocardial Ischemia/metabolism/pathology/physiopathology; Myocardium/metabolism/pathology; Necrosis; Oligonucleotide Probes; RNA, Messenger/biosynthesis; Rats; Rats, Sprague-Dawley; Retroviridae Proteins, Oncogenic/biosynthesis; Time Factors; Transcription Factors; Transcription, Genetic
Abstract :
[en] Ischaemic injury leads to the expression of heat shock and immediate early genes. Here the localization of this induction is examined by in situ hybridization analysis in serial sections of buffer-perfused isolated rat heart after 30 min of coronary artery occlusion. The accumulation of mRNA for hsc70, hsp70, c-fos, c-jun, and Erg-1 was localized coincidently and was restricted to the ischaemic area of the heart. mRNA for these genes was undetectable at the end of the ischaemic period (no reperfusion). After 30 min of reperfusion, accumulation of mRNA for hsc70, hsp70, c-fos, and c-jun was detectable and increased with further reperfusion. Within the area labelled for these gene products was a central area of less intense labelling which corresponded to the necrotic zone. The immediate early gene product, jun-B, was localized in both the ischaemic and the non-ischaemic area of the hearts. These results suggest that the area of the heart where heat shock and immediate early gene transcripts accumulate, while injured, recovers transcriptional activity, and that the central area where minimal heat shock and immediate early gene transcripts accumulate, does not recover transcriptional activity and is irreversibly injured.
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