Late ischemic preconditioning of the myocardium alters the expression of genes involved in inflammatory response

被引:20
作者
Zubakov, D
Hoheisel, JD
Kluxen, FW
Brändle, M
Ehring, T
Hentsch, B
Frohme, M
机构
[1] Deutsch Krebsforschungszentrum, German Canc Res Ctr, Funct Genome Anal, D-69120 Heidelberg, Germany
[2] Mersk KGaA, Biomed Res CADS, D-64271 Darmstadt, Germany
关键词
heart; preconditioning; gene expression; representational difference analysis; microarray;
D O I
10.1016/S0014-5793(03)00667-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Myocardial ischemic preconditioning (IPC) is a potent endogenous mechanism of cardioprotection against ischemia-reperfusion injury. In this study we focused on the second phase of IPC as the most interesting in terms of therapeutic implementations. We aimed at the detection of genes, which are differentially expressed at 16 h after reperfusion. Preconditioning of canine myocardium was initiated by 5 min occlusion of the left anterior descending coronary artery with subsequent reperfusion. cDNA representational difference analysis in combination with microarray hybridization and reverse transcription polymerase chain reaction were used to reveal the changes in gene expression in canine hearts. We found that functionally related genes for tristetraproline (TTP), selectin E, matrix metalloproteinase 9, and tumor necrosis factor-a were highly upregulated at the late phase of IPC. The upregulation of TTP gene at the late phase of IPC, reported here for the first time, may represent a cardioprotective mechanism, which could be a promising perspective in clinical interventions against ischemia-reperfusion injuries of the heart. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:51 / 55
页数:5
相关论文
共 36 条
[1]  
ALTSCHUL SF, 1990, J MOL BIOL, V215, P403, DOI 10.1006/jmbi.1990.9999
[2]   Delayed preconditioning of myocardium: current perspectives [J].
Baxter, GF ;
Ferdinandy, P .
BASIC RESEARCH IN CARDIOLOGY, 2001, 96 (04) :329-344
[3]   The late phase of preconditioning [J].
Bolli, R .
CIRCULATION RESEARCH, 2000, 87 (11) :972-983
[4]   Transcriptional arrest of the human E-selectin gene [J].
Boyle, EM ;
Sato, TT ;
Noel, RF ;
Verrier, ED ;
Pohlman, TH .
JOURNAL OF SURGICAL RESEARCH, 1999, 82 (02) :194-200
[5]   Feedback inhibition of macrophage tumor necrosis factor-α production by tristetraprolin [J].
Carballo, E ;
Lai, WS ;
Blackshear, PJ .
SCIENCE, 1998, 281 (5379) :1001-1005
[6]   Decreased sensitivity of tristetraprolin-deficient cells to p38 inhibitors suggests the involvement of tristetraprolin in the p38 signaling pathway [J].
Carballo, E ;
Cao, HP ;
Lai, WS ;
Kennington, EA ;
Campbell, D ;
Blackshear, PJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (45) :42580-42587
[7]   E-selectin gene expression in vascular smooth muscle cells - Evidence for a tissue-specific repressor [J].
Chen, XLL ;
Tummala, PE ;
Olliff, L ;
Medford, RM .
CIRCULATION RESEARCH, 1997, 80 (03) :305-311
[8]   Manufacturing DNA microarrays of high spot homogeneity and reduced background signal [J].
Diehl, Frank ;
Grahlmann, Susanne ;
Beier, Markus ;
Hoheisel, Joerg D. .
NUCLEIC ACIDS RESEARCH, 2001, 29 (07)
[9]   TUMOR-NECROSIS-FACTOR-ALPHA PRETREATMENT IS PROTECTIVE IN A RAT MODEL OF MYOCARDIAL ISCHEMIA-REPERFUSION INJURY [J].
EDDY, LJ ;
GOEDDEL, DV ;
WONG, GHW .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 184 (02) :1056-1059
[10]   Myocardial and interstitial matrix metalloproteinase activity after acute myocardial infarction in pigs [J].
Etoh, T ;
Joffs, C ;
Deschamps, AM ;
Davis, J ;
Dowdy, K ;
Hendrick, J ;
Baicu, S ;
Mukherjee, R ;
Manhaini, M ;
Spinale, FG .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2001, 281 (03) :H987-H994