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The Study of Endothelial-Mesenchymal Transition in an Atrial Fibrillation Rat Model
Background:
Activated fibroblasts are reported partly of endothelial origin, derived through endothelial-mesenchymal transition (EndMT). Few studies have investigated EndMT in atrial fibrillation (AF), which may have a potential effect on cardiac fibrosis.
Objective:
To investigate whether EndMT occurs in an animal model of AF.
Methods:
A total of 80 Sprague‒Dawley rats (8 weeks, male, 200-250 g) were randomly divided into two groups: the control group and the AF group (n = 40 in each group). Rats in the AF group received a daily intravenous injection of acetylcholine-calcium chloride for seven days to establish an AF model, and rats in the control rats were injected with saline in the same way. At different time points (Day 3, Day 5, Day 7, Day 9, Day 11, Day 13, Day 15, and Day 17), we observed changes in EndMT-related indexes (CD31, VE-cadherin, FSP-1, TGF-β1 and collagen) and HIF-1α in the rat atria of two groups, as well as immunofluorescence co-expression of CD31/FSP-1 and VE-cadherin/FSP-1 in the endocardial endocardium of the atria.
Results:
In the AF group, atrial EndMT was observed and enhanced with time. Compared with the control group, the levels of CD31 and VE-cadherin in the AF group decreased, while mesenchymal marker (FSP-1) and EndMT inducer (TGF-β1) were dynamically increased after Day 3. The co-expression of CD31/FSP-1 and VE-cadherin/FSP-1 was observed from Day 3 to the end of observation time Day 17 by immunofluorescence in AF rat hearts, indicating the existence of EndMT. In addition, the level of HIF-1α in the hearts of AF rats was increased.
Conclusion:
As far as we know, this is the first study to explore the dynamic process of EndMT in an AF rat model. The presence of EndMT was verified in the atria of the AF rat model, and Day 7-Day 17 was the best observation time point for the model. This may lead to a better understanding of the pathological changes and mechanisms in AF with a short modeling cycle.
