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The HL‐1 cardiomyocyte cell line exhibits store‐operated calcium entry
Author(s) -
Touchberry Chad,
Elmore Chris,
Nguyen Tien,
Andresen Jon,
Zhao Xiaoli,
Orange Matthew,
Weisleder Noah,
Brotto Marco,
Claycomb William,
Wacker Michael
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1112.11
Subject(s) - orai1 , stim1 , microbiology and biotechnology , chemistry , myocyte , voltage dependent calcium channel , gene knockdown , cell type , cell culture , calcium signaling , cell , calcium , signal transduction , biology , endoplasmic reticulum , biochemistry , genetics , organic chemistry , apoptosis
Store‐operated Ca 2+ entry (SOCE) has been observed in many cell types, but only recently has it been shown to be of physiological importance in cardiomyocytes. Because of the increasing importance of SOCE in cardiomyocytes, its important role in maladaptive hypertrophy, and the difficulty in studying SOCE currents in primary myocytes, we sought to test the utility of the HL‐1 cell line as a model to study SOCE. We report for the first time that these cells express stromal interaction molecule 1 (STIM1) and the Ca 2+ release‐activated Ca 2+ (CRAC) channel, Orai1 at the mRNA and protein level. In addition, HL‐1 cells respond to SR‐Ca 2+ depletion by initiating a SOCE response, that was not prevented by inhibition of L‐type channels, T‐type channels or the reverse mode Na + /Ca 2+ exchanger (NCX). We were able to eliminate SOCE with known SOCE inhibitors (BTP‐2 and SKF‐96365) and by targeted knockdown of Orai1. Currently, there is little knowledge about SOCE in cardiomyocytes, and the present results suggest that HL‐1 cells will be of great utility in investigating the role of SOCE in the heart.