Referenced in: none

Automatically associated channels: Slo1

Title: Different effects of lysophosphatidic acid on L-type calcium current in neonatal rat ventricular myocytes with and without H2O2 treatment.

Authors: Renren Sun, Duoduo Zhang, Jun Zhang, Qiuyan Feng, Yan Zhang, Chunyan Zhao, Wenjie Zhang

Journal, date & volume: Prostaglandins Other Lipid Mediat., 2015 Apr-Jun , 118-119, 1-10

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25841350

Abstract
L-type calcium current (I(Ca-L)) alterations are implicated in various cardiac diseases, and the lysophosphatidic acid (LPA) level increases in several ischemic heart diseases. We investigated the effects of LPA on I(Ca-L) in normal and H2O2-treated neonatal rat ventricular myocytes. LPA treatment (24h) increased the action potential duration (APD) and I(Ca-L) in normal ventricular myocytes, but it decreased these parameters in H2O2-treated myocytes. LPA increased the single-channel open probability of L-type calcium channels in both normal and H2O2-treated myocytes. LPA activated calcineurin (CaN) and induced the cytoplasm-to-nucleus translocation of nuclear factor of activated T-cells (NFAT) in H2O2-treated cardiomyocytes. In H2O2-treated cardiomyocytes, LPA decreased Ca(v)1.2 mRNA and protein expression levels at 4 and 8h, respectively. A CaN inhibitor (FK-506) prevented LPA-induced APD, I(Ca-L), and Ca(v)1.2 mRNA and protein down-regulation. The LPA-induced I(Ca-L) increase in normal cardiomyocytes was CaN-NFAT signaling-independent, and LPA did not affect Ca(v)1.2 mRNA or protein expression. In conclusion, LPA increases the I(Ca-L) in normal ventricular myocytes by increasing the single-channel open probability of L-type calcium channels, and LPA decreases I(Ca-L) in H2O2-treated cardiomyocytes via the CaN-NFAT pathway.