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L. V. Mayne,T. J. Pell, G. F. Baxter,D. M. Yellon,D. S. Latchman,M. F. Hubank,M.A.C. Fauchon,G. F. Baxter 생화학분자생물학회 2005 Experimental and molecular medicine Vol.37 No.4
Preconditioning of the myocardium rapidly induces a number of transcription factors, which are likely to be responsible for a cascade of transcriptional changes underlying the development of delayed adaptation. Identifying these changes provides in-sight into the molecular pathways elicited by delayed adaptation. Genes up-regulated in rabbit myocardium in vivo by ischaemic preconditioning following reperfusion for 2 h, 4 h and 6 h post- treatment were identified by representational dif-ference analysis of cDNA (cDNA. RDA). The area of the left ventricle rendered ischaemic by precon-ditioning or the equivalent area of sham-treated animals was isolated and cDNA.RDA performed. Three novel genes and six genes with known function where identified, including the TGFβ receptor interacting protein 1, the α isoform of the A subunit of PP2 and the cap binding protein NCBP1. To determine whether expression of these genes correlated with preconditioning per se, expression was measured in myocardium after both ischaemic as well as heat shock induced preconditioning following 2 h, 4 h, and 6 h reperfusion. These genes were induced in rabbit myocardium in vivo by both ischaemia and heat shock, consistent with a fundamental role in the development of delayed adaptation. The well described role of PP2 in modulating the mitogen-activated protein kinase pathway and promoting cell survival is consistent with our previous work, which identified the reper-fusion injury salvage kinase pathway in mediating the protective effects of ischaemic preconditioning. Expression of Trip1 and Ncbp1 also implicates TGFβ signalling pathways and RNA processing and transport in delayed adaptation to stress in the myocardium.