Comparison of changes in left ventricular gene expression profiles from different cardiac hypertrophy models in rats.
- Author:
Ping LI
1
;
Jin-Liang LI
;
Xin-Heng FENG
;
Zhao-Ping LI
;
Feng YIN
;
Jie YAN
;
Rong HOU
;
Qi-De HAN
;
You-Yi ZHANG
Author Information
1. Institute of Vascular medicine, peking university third hospital and Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100083, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Aorta, Abdominal;
surgery;
Arteriovenous Shunt, Surgical;
Cardiomegaly;
etiology;
genetics;
Constriction;
Gene Expression Profiling;
Male;
Myocytes, Cardiac;
drug effects;
metabolism;
Norepinephrine;
Oligonucleotide Array Sequence Analysis;
Oligonucleotide Probes;
Random Allocation;
Rats;
Rats, Wistar;
Venae Cavae;
surgery
- From:
Acta Physiologica Sinica
2004;56(2):210-218
- CountryChina
- Language:Chinese
-
Abstract:
To get insights into the principles of gene expression changes during cardiac hypertrophy, three rat cardiac hypertrophy models were prepared, i.e., suprarenal abdominal aortic stenosis (SRS), arterial-vein fistula (AVF) and continuous jugular vein infusion of norepinephrine (NEi). The cardiac function and structure were analyzed by echocardiograph as well as histological examination. Total RNA of left ventricles was extracted and gene expression profiles were analyzed by cDNA microarray. SRS and NEi induced concentric cardiac hypertrophy and AVF induced eccentric hypertrophy in rats, among which NEi caused obvious cardiac fibrosis. The changes of gene expression profiles were compared comprehensively across different pathologic cardiac hypertrophy models. While gene expression profiles of different cardiac hypertrophy models compared with pairs, parts of the genes involved were found overlapped, and mostly the gene expression changed in the same direction between two models, but some of them changed in the opposite directions. Expression levels of 19 genes were found changed across all cardiac hypertrophy models, and genes relatively regulated in a specific model was also found when comparison of all the three models was carried out. Novel clues for further study might derive from the results mentioned above, and some genes might be the marker genes of cardiac hypertrophy or the targets of therapy.
