Mice with endothelial cell ‐selective adhesion molecule deficiency develop coronary microvascular rarefaction and left ventricle diastolic dysfunction

Endothelial cell-selective adhesion molecule (ESAM) regulates inflammatory cell adhesion and transmigration and promotes angiogenesis. We propose that animals deficient in ESAM develop left ventricular diastolic dysfunction due to reduced myocardial vascular density, hypoxia, and inflammation. Hemodynamic challenge lead to worsening of left ventricular diastolic dysfunction in ESAM knockout mice. AbstractEndothelial cell-selective adhesion molecule (ESAM) regulates inflammatory cell adhesion and transmigration and promotes angiogenesis. Here, we examined the role of ESAM in cardiac vascularization, inflammatory cell infiltration, and left ventricle (LV) diastolic function under basal and hemodynamic stress conditions. We employed mice with homozygous genetic deletion of ESAM (ESAM−/−) and also performed uninephrectomy and aldosterone infusion (UNX-Aldo) to induce volume and pressure overload. Using echocardiography, we found that ESAM−/− mice display no change in systolic function. However, they develop LV diastolic dysfunction, as indicated by a significantly reduced E/A ratio (E  = early, A = late mitral inflow peak velocities), increased E/e’ ratio, isovolumic relaxation time (IVRT), and E wave deceleration time. An unbiased automated tracing and 3D reconstruction of coronary vasculature revealed that ESAM−/− mice had reduced coronary vascular density. Arteries of ESAM−/− mice exhibited impaired endothelial sprouting and in cultured endothelial cells ...

Source: Physiological Reports - March 22, 2023 Category: Physiology Authors: Vadym Buncha, Katie Anne Fopiano, Liwei Lang, Celestine Williams, Anatolij Horuzsko, Jessica Andrea Filosa, Gaston Kapuku, Zsolt Bagi Tags: ORIGINAL ARTICLE Source Type: research