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(Hypertension. 2001;38:1062.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Angiotensin II via Activation of Type 1 Receptor Upregulates Expression of Endoglin in Human Coronary Artery Endothelial Cells

Dayuan Li; Hongjiang Chen; Jawahar L. Mehta

From the Departments of Internal Medicine and Physiology, University of Arkansas for Medical Sciences, and the Central Arkansas Veterans Healthcare System, Little Rock.

Correspondence to J.L. Mehta, MD, PhD, Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, 4301 West Markham St, Mail Slot 532, Little Rock, AR 72205-7199. E-mail MehtaJL{at}uams.edu

Abstract—— Transforming growth factor-ß1 and its subtype receptor endoglin are key components in angiogenesis. We explored the role of angiotensin (Ang) II in the expression of endoglin and the underlying intracellular signaling mechanism in human coronary artery endothelial cells. Incubation of cells with Ang II upregulated endoglin expression in a concentration- and time-dependent manner (maximal effect with 10^-6 mol/L Ang II at 24 hours). The Ang II type 1 receptor blocker losartan, but not the type 2 receptor blocker PD 123,319, completely blocked the effect of Ang II. In parallel experiments, the mitogen-activated protein kinase inhibitor PD 098,059 fully inhibited the effect of Ang II on the expression of endoglin. Incubation of endothelial cells with Ang II also increased the expression of transforming growth factor-ß1 and -ß2 receptors and simultaneously decreased the levels of transforming growth factor-ß1. These effects of Ang II were also attenuated by losartan. We propose that Ang II via its type 1 receptor activation modulates the expression of transforming growth factor-ß1 receptors in human coronary endothelial cells. The activation of mitogen-activated protein kinase plays an important role in this process. These observations provide a new clue regarding the regulatory effect of Ang II on vascular remodeling after injury.

Key Words: angiotensin II • endothelium • transforming growth factors • protein kinases

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