Endothelial-derived extracellular vesicles from obese/hypertensive adults increase factors associated with hypertrophy and fibrosis in cardiomyocytes

Author:

Fandl Hannah K.1ORCID,Garcia Vinicius P.1,Treuth John W.1,Brewster Lillian M.1ORCID,Greiner Jared J.1,Davy Kevin P.2,Stauffer Brian L.34,Desouza Christopher A.14ORCID

Affiliation:

1. Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, Colorado, United States

2. Human Integrative Physiology Laboratory, Department of Human Nutrition, Foods, and Exercise, Virginia Tech University, Blacksburg, Virginia, United States

3. Division of Cardiology, Denver Health Medical Center, Denver, Colorado, United States

4. Division of Cardiology, Anschutz Medical Center, University of Colorado, Denver, Colorado, United States

Abstract

In the present study we determined the effect of endothelial microvesicles (EMVs) isolated from obese/hypertensive adults on mediators of cardiomyocyte hypertrophy [cardiac troponin T (cTnT), α-actinin, nuclear factor-kB (NF-kB)] and fibrosis [transforming growth factor (TGF-β), collagen1-α1] as well as endothelial nitric oxide synthase (eNOS) expression and NO production. EMVs from obese/hypertensive induced significantly higher expression of hypertrophic (cTnT, α-actinin, NF-kB) and fibrotic (TGF-β) proteins as well as significantly lower eNOS activation and NO production in cardiomyocytes than EMVs from normal weight/normotensive adults. EMVs are a potential mediating factor in the increased risk of cardiomyopathy and heart failure with obesity/hypertension.

Funder

HHS | NIH | National Center for Advancing Translational Sciences

HHS | NIH | National Heart, Lung, and Blood Institute

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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