[Differential gene expression profile in ischemic myocardium of Wistar rats with acute myocardial infarction: the study on gene construction, identification and function].
OBJECTIVE
To construct the differential genes expressed profile in the ischemic myocardium tissue reduced from acute myocardial infarction(AMI), and determine the biological functions of target genes.


METHODS
AMI model was generated by ligation of the left anterior descending coronary artery in Wistar rats. Total RNA was extracted from the normal and the ischemic heart tissues under the ligation point 7 days after the operation. Differential gene expression profiles of the two samples were constructed using Long Serial Analysis of Gene Expression(LongSAGE). Real time fluorescence quantitative PCR was used to verify gene expression profile and to identify the expression of 2 functional genes. The activities of enzymes from functional genes were determined by histochemistry.


RESULTS
A total of 15,966 tags were screened from the normal and the ischemic LongSAGE maps. The similarities of the sequences were compared using the BLAST algebra in NCBI and 7,665 novel tags were found. In the ischemic tissue 142 genes were significantly changed compared with those in the normal tissue (P<0.05). These differentially expressed genes represented the proteins which might play important roles in the pathways of oxidation and phosphorylation, ATP synthesis and glycolysis. The partial genes identified by LongSAGE were confirmed using real time fluorescence quantitative PCR. Two genes related to energy metabolism, COX5a and ATP5e, were screened and quantified. Expression of two functional genes down-regulated at their mRNA levels and the activities of correlative functional enzymes decreased compared with those in the normal tissue.


CONCLUSIONS
AMI causes a series of changes in gene expression, in which the abnormal expression of genes related to energy metabolism could be one of the molecular mechanisms of AMI. The intervention of the expressions of COX5a and ATP5e may be a new target for AMI therapy.
Guo
Chun Yu
CY
Cardiovascular Center, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
Yin
Hui Jun
HJ
Jiang
Yue Rong
YR
Xue
Mei
M
Zhang
Lu
L
Shi
Da Zhuo
da Z
D000818:Animals; D003576:Electron Transport Complex IV / Q000235:genetics; D020869:Gene Expression Profiling; D008297:Male; D009203:Myocardial Infarction / Q000235:genetics*; D009206:Myocardium / Q000378:metabolism*; D011506:Proteins / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D000097795:ATPase Inhibitory Protein
D003576:Electron Transport Complex IV; D011506:Proteins; D000097795:ATPase Inhibitory Protein