BC2M participation in SFD

March 21-24, 2024 at the Montpellier Exhibition Centre

With Anne Dominique LAJOIX, member of the Scientific Committee
and Mohammed MIMOUNI, who gave an oral presentation summarized below:

The metabolic syndrome, a combination of insulin resistance and high blood pressure, leads to early remodeling of the myocardium, particularly of the extracellular matrix, resulting in interstitial fibrosis. Our team has previously demonstrated, in an animal model of metabolic syndrome, that a salt-depleted diet is capable of preventing these cardiac lesions. A transcriptomics study identified several genes modulated by sodium restriction. To better understand the role of these genes, we set up two in vitro models of endothelial-mesenchymal transition, mimicking early myocardial remodeling using primary human endothelial cells. Materials and Methods Primary human aortic endothelial cells (HAEC), and human umbilical vein endothelial cells (HUVEC) are treated at different times with TGF-β2 (10ng/ml). Expression of endothelial and mesenchymal markers, as well as various genes, was demonstrated by q-PCR, Western blot and immunofluorescence. Results In both cell types, TGF-β2 significantly increased expression of the mesenchymal markers SM22-α, Snail, Slug, with increased phosphorylation of Smad2/3. Collagen expression is observed only in HAECs, reflecting earlier transdifferentiation. Expression of the endothelial markers Pecam-1 and VE-Cadherin appeared unchanged in both cases. In immunofluorescence, the 2 cell types coexpressed Pecam-1 and SM22-α, reflecting their transdifferentiation into fibroblastic cells. In these 2 models, several genes are overexpressed during transdifferentiation, such as latrophilin-1, which is involved in cell adhesion, and fibulin-5, an extracellular matrix protein, 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 during metabolic syndrome.

Link to the SFD website here.