Abstract
Store-operated Ca2+ 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 Ca2+ release-activated Ca2+ (CRAC) channel, Orai1 at the mRNA and protein level. In addition, HL-1 cells respond to SR-Ca2+ depletion by initiating a SOCE response, that was not prevented by inhibition of L-type channels, T-type channels or the reverse mode Na+/Ca2+ 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
