Comparison of Phenotype and Signal Pathway in Experimental Mouse Models of Cardiac Fibrosis Induced by ISO and AngII
ZHOU Wenhui1, WANG Bo2, XIA Sheng1*
The aim of the study was to critically evaluate the available evidence regarding the difference between mouse models of cardiac fibrosis induced by ISO (isoprenaline) and AngII (angiotensin II). C57 wild type mice were randomly divided into ISO group, AngII group and NS (normal saline) control group. Mice in ISO model group were given subcutaneous injection of ISO. Mice in AngII model group were treated with AngII infusion via an implanted osmotic minipump. The mice of control group were administered normal saline in the same way. After 28 days, cardiac function and fibrosis were evaluated by echocardiography, micromanometry, histology and CWI (cardiac weight index). The results showed that there were no difference in cardiac function between ISO and AngII models in terms of cardiac function. However, mice receiving ISO displayed more severe cardiac fibrosis, lower vein systolic pressure and CWI compared with mice receiving AngII. Importantly, the different signaling pathways activated in the two models were found. These findings indicate that pathological change of cardiac fibrosis induced by ISO model is severer than that in AngII model through different signaling pathway.
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