Potential effect of resistin on the ET-1-increased reactions of blood pressure in rats and Ca2+ signaling in vascular smooth muscle cells
✍ Scribed by Tung-Yueh Chuang; Lo-Chun Au; Li-Chun Wang; Low-Tone Ho; De-Ming Yang; Chi-Chang Juan
- Publisher
- John Wiley and Sons
- Year
- 2012
- Tongue
- English
- Weight
- 441 KB
- Volume
- 227
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
Resistin and endothelin‐1 (ET‐1) are upregulated in people with type II diabetes mellitus, central obesity, and hypertension. ET‐1 signaling is involved in Ca^2+^‐contraction coupling and related to blood pressure regulation. The aim of this study is to investigate the role of resistin on ET‐1‐increased blood pressure and Ca^2+^ signaling. The blood pressure and cytosolic Ca^2+^ of vascular smooth muscle cells (VSMCs) of Sprague–Dawley rats were detected. The data demonstrated that resistin accelerated and prolonged ET‐1‐induced increases in blood pressure and had significant effects on ET‐1‐increased Ca^2+^ reactions. Resistin‐enhanced ET‐1‐increased Ca^2+^ reactions were reversed by blockers of store‐operated Ca^2+^ entry (SOCE) and extracellular‐signal‐regulated kinase (ERK). The endogenous expression of Orai and stromal interaction molecular (STIM) were characterized in the VSMCs. Furthermore, resistin‐enhanced ET‐1 Ca^2+^ reactions and the resistin‐dependent activation of SOCE were abolished under STIM1‐siRNA treatment, indicating that STIM1 plays an important role in resistin‐enhanced ET‐1 Ca^2+^ reactions in VSMCs. Resistin appears to exert effects on ET‐1‐induced Ca^2+^ increases by enhancing the activity of ERK‐dependent SOCE (STIM1‐partcipated), and may accelerate and prolong ET‐1‐increased blood pressure via the same pathway. J. Cell. Physiol. 227: 1610–1618, 2012. © 2011 Wiley Periodicals, Inc.