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Potential effect of resistin on the ET‐1‐increased reactions of blood pressure in rats and Ca 2+ signaling in vascular smooth muscle cells
Author(s) -
Chuang TungYueh,
Au LoChun,
Wang LiChun,
Ho LowTone,
Yang DeMing,
Juan ChiChang
Publication year - 2012
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22878
Subject(s) - resistin , endocrinology , medicine , blood pressure , vascular smooth muscle , chemistry , cytosol , extracellular , signal transduction , microbiology and biotechnology , biology , biochemistry , diabetes mellitus , insulin resistance , smooth muscle , adipokine , enzyme
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.