p2x4 receptor–enos signaling pathway in cardiac myocytes as a novel protective mechanism in heart failure

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ID: 204937
2015
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Abstract
We have demonstrated using immunoprecipitation and immunostaining a novel physical association of the P2X4 receptor (P2X4R), a ligand-gated ion channel, with the cardioprotective, calcium-dependent enzyme endothelial nitric oxide synthase (eNOS). Treatment of murine ventricular myocytes with the P2XR agonist 2-methylthioATP (2-meSATP) to induce a current (mainly Na+) increased the formation of nitric oxide (NO), as measured using a fluorescent probe. Possible candidates for downstream effectors mediating eNOS activity include cyclic GMP and PKG or cellular protein nitrosylation. A cardiac-specific P2X4R overexpressing mouse line was protected from heart failure (HF) with improved cardiac function and survival in post-infarct, pressure overload, and calsequestrin (CSQ) overexpression models of HF. Although the role of the P2X4R in other tissues such as the endothelium and monocytes awaits characterization in tissue-specific KO, cardiac-specific activation of eNOS may be more cardioprotective than an increased activity of global systemic eNOS. The intra-myocyte formation of NO may be more advantageous over NO derived externally from a donor. A small molecule drug stimulating this sarcolemmal pathway or gene therapy-mediated overexpression of the P2X4R in cardiac myocytes may represent a new therapy for both ischemic and pressure overloaded HF.
Reference Key
yang2015computationalp2x4 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Ronghua Yang, Dardan Beqiri, Jian-Bing Shen, John M. Redden, Kimberly Dodge-Kafka, Kenneth A. Jacobson, Bruce T. Liang
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Journal ceramics international
Year 2015
DOI
10.1016/j.csbj.2014.11.002
URL
http://www.sciencedirect.com/science/article/pii/S2001037014000439
Keywords
cardioprotection

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