Loss of adropin causes arterial stiffening in mouse femoral and mesenteric arteries

Abstract

Adropin is a 76-amino acid hormone encoded by the Enho gene and primarily known for its role in the regulation of energy homeostasis. It is expressed in multiple tissues including the vasculature. In endothelial cells, adropin promotes eNOS activation and exerts vasodilatory effects. Studies in humans demonstrate that adropin levels in circulation are depressed with aging, obesity, and type 2 diabetes, all of which are conditions characterized by increased arterial stiffness, an independent risk factor for cardiovascular disease. Herein, we tested the hypothesis that loss of adropin is implicated in arterial stiffening. To test this hypothesis, we used ~25-week-old adropin knockout (n=14) and wild-type (n=9) littermate male mice fed a standard chow diet. Pressure myography was utilized to determine the elastic properties of isolated femoral and mesenteric arteries under passive conditions. We report that adropin knockout mice exhibited a greater incremental moduli of elasticity in both femoral and mesenteric arteries (a higher value is indicative of a stiffer vessel), relative to wild-type mice (P<0.05). These differences were independent of any changes in body weight or glucose control. The current findings support the hypothesis that lack of adropin is sufficient to cause arterial stiffening. Follow up experiments are underway to identify the possible mechanisms.