BC2M's Participation in SFD

March 21–24, 2024, at the Montpellier Exhibition Center

With Anne Dominique LAJOIX, member of the scientific committee
and Mohammed MIMOUNI, who gave an oral presentation, a summary of which is provided below:

Metabolic syndrome, which involves insulin resistance and high blood pressure, leads to early myocardial remodeling, particularly of the extracellular matrix, which triggers the development of interstitial fibrosis. Our team has previously demonstrated in an animal model of metabolic syndrome that a low-salt diet is capable of preventing these cardiac lesions. A transcriptomic study identified several genes modulated by sodium restriction. To better understand the role of these genes, we established two in vitro models of endothelial-mesenchymal transition, replicating early myocardial remodeling using primary human endothelial cells. Materials and Methods Primary human aortic endothelial cells (HAEC) and human umbilical vein endothelial cells (HUVEC) were treated at different time points with TGF-β2 (10 ng/ml). The expression of endothelial and mesenchymal markers, as well as various genes, was assessed by q-PCR, Western blot, and immunofluorescence. Results In both cell types, TGF-β2 significantly increased the expression of the mesenchymal markers SM22-α, Snail, and Slug, accompanied by increased Smad2/3 phosphorylation. Collagen expression was observed only in HAECs, indicating earlier transdifferentiation. The expression of the endothelial markers Pecam-1 and VE-Cadherin appears unchanged in both cases. By immunofluorescence, both cell types co-express Pecam-1 and SM22-α, indicating their transdifferentiation into fibroblastic cells. In these two models, several genes are overexpressed during transdifferentiation, such as latrophilin-1, which is involved in cell adhesion, and fibulin-5, an extracellular matrix protein, thereby confirming the results observed in our animal model. Conclusion We have established two cellular models of endothelial-mesenchymal transition that can be used to study early myocardial remodeling in metabolic syndrome.

Click here to visit the SFD website.