Gene expression profile in mouse myocardium after ischemia

被引:76
作者
Lyn, D
Liu, XW
Bennett, NA
Emmett, NL
机构
[1] Morehouse Sch Med, Dept Biochem, Atlanta, GA 30310 USA
[2] Morehouse Sch Med, Dept Physiol, Atlanta, GA 30310 USA
[3] Morehouse Sch Med, Cardiovasc Inst, Atlanta, GA 30310 USA
关键词
complementary deoxyribonucleic acid array; coronary artery occlusion; myosin; p18ink4; transcription factors;
D O I
10.1152/physiolgenomics.2000.2.3.93
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
This study was designed to elaborate a molecular profile of expressed genes during ischemic injury to the mouse heart after surgical constriction of the left coronary artery without reperfusion. A mouse cDNA array containing 588 known genes was used to compare gene expression in heart RNA after 24-h ischemia with control tissue. Alterations in gene expression on the array were supported by relative reverse transcription-polymerase chain reaction analysis after timed periods of ischemia. Decreased levels of the cell cycle regulator p18ink4 and the oxidative responsive gene glutathione S-transferase were accompanied by an upregulation of the genes associated with cardiac muscle development, alpha-myosin heavy chain and fetal myosin alkali light chain. Other stress responses elicited by cardiac injury included an induction of Egr-1 and Egr-3 transcription factors, as well as the apoptotic regulator Bax. Altogether, these findings indicate that expression of genes associated with a fetal transcription program may be involved with the post ischemic remodeling process in heart ventricles.
引用
收藏
页码:93 / 100
页数:8
相关论文
共 31 条
[1]   Quantification of cardioprotective gene expression in porcine short-term hibernating myocardium [J].
Bartling, B ;
Hoffmann, J ;
Holtz, J ;
Schulz, R ;
Heusch, G ;
Darmer, D .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1999, 31 (01) :147-158
[2]   MOLECULAR SIGNALING MECHANISMS CONTROLLING GROWTH AND FUNCTION OF CARDIAC FIBROBLASTS [J].
BOOZ, GW ;
BAKER, KM .
CARDIOVASCULAR RESEARCH, 1995, 30 (04) :537-543
[3]   PROTOONCOGENE EXPRESSION IN PORCINE MYOCARDIUM SUBJECTED TO ISCHEMIA AND REPERFUSION [J].
BRAND, T ;
SHARMA, HS ;
FLEISCHMANN, KE ;
DUNCKER, DJ ;
MCFALLS, EO ;
VERDOUW, PD ;
SCHAPER, W .
CIRCULATION RESEARCH, 1992, 71 (06) :1351-1360
[4]   Physiological assessment of complex cardiac phenotypes in genetically engineered mice [J].
Christensen, G ;
Wang, YB ;
Chien, KR .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 272 (06) :H2513-H2524
[5]   GENE-EXPRESSION IN ACUTE MYOCARDIAL STRESS - INDUCTION BY HYPOXIA, ISCHEMIA, REPERFUSION, HYPERTHERMIA AND OXIDATIVE STRESS [J].
DAS, DK ;
MAULIK, N ;
MORARU, II .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (01) :181-193
[6]   Metabolic derangement in ischemic heart disease and its therapeutic control [J].
Ferrari, R ;
Pepi, P ;
Ferrari, F ;
Nesta, F ;
Benigno, M ;
Visioli, O .
AMERICAN JOURNAL OF CARDIOLOGY, 1998, 82 (5A) :2K-13K
[7]  
Goldman S, 1995, J Card Fail, V1, P169, DOI 10.1016/1071-9164(95)90019-5
[8]   Apoptosis in myocardial ischemia-reperfusion [J].
Gottlieb, RA ;
Engler, RL .
HEART IN STRESS, 1999, 874 :412-426
[9]  
GUPTA MP, 1991, J BIOL CHEM, V266, P12813
[10]   INHIBITION BY ANGIOTENSIN-II TYPE-1 RECEPTOR ANTAGONIST OF CARDIAC PHENOTYPIC MODULATION AFTER MYOCARDIAL-INFARCTION [J].
HANATANI, A ;
YOSHIYAMA, M ;
KIM, SK ;
OMURA, T ;
TODA, I ;
AKIOKA, K ;
TERAGAKI, M ;
TAKEUCHI, K ;
IWAO, H ;
TAKEDA, T .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1995, 27 (09) :1905-1914