Kyotani, Yoji and Zhao, Jing and Ozawa, Kentaro and Nakagawa, Takahiko and Bolstad, Francesco A. and Yoshizumi, Masanori (2016) Endothelin-1 (1-31) Causes the Migration of Vascular Smooth Muscle Cells through Endothelin ETA Receptor. British Journal of Pharmaceutical Research, 13 (6). pp. 1-7. ISSN 22312919
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Abstract
Endothelin-1 (ET-1) is predominantly expressed in endothelial cells to modulate physiological actions, such as vasoconstriction and cell proliferation. It acts as an autocrine and paracrine factor, and has been reported to be found in increased levels in the blood of patients with hyperlipidemia and atherosclerosis. The excessive proliferation and migration of vascular smooth muscle cells (VSMCs) characterize the progression of atherosclerosis. Thus, ET-1 is currently believed to be an important factor for atherosclerosis. Endothelin-1 (1-31) is a relatively recently discovered form of ET and is generated from big ET-1 by chymase, which is predominantly expressed in mast cells. Recently, the elevated concentration of circulating ET-1 (1-31) in patients with acute myocardial infarction has been reported. In this study, we investigated whether ET-1 (1-31) could induce VSMC migration and compared its effect with that of ET-1. ET-1 (1-31) significantly stimulated rat aortic vascular smooth muscle cell (RASMC) migration in a concentration dependent manner. ET-1 (1-31) at 100 nM caused a 1.38-fold increase in RASMC migration whereas ET-1 at the same concentration resulted in a 1.60-fold increase. The ET-1 (1-31)-stimulated RASMC migration was significantly inhibited by BQ123, a specific ETA receptor antagonist, but not by BQ788, a specific ETB receptor antagonist. These data suggest that ET-1 (1-31) stimulates the VSMC migration through ETA receptors but not ETB receptors. The findings presented in this paper bring us one step closer to understanding the mechanisms involved in atherosclerosis.
Item Type: | Article |
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Subjects: | Open Archive Press > Medical Science |
Depositing User: | Unnamed user with email support@openarchivepress.com |
Date Deposited: | 17 Jun 2023 05:40 |
Last Modified: | 04 Mar 2024 05:25 |
URI: | http://library.2pressrelease.co.in/id/eprint/1408 |