Abstract
Alcoholic cardiomyopathy is one of the leading causes of non‐ischemic dilated cardiomyopathy accounting for 36% of cases. Almost 50% of alcoholics develop this disease. Previously our lab has demonstrated the up‐regulation of intracellular Ca2+ (IC) in dilated cardiomyopathy by Akt. Here we investigate the role of Akt in regulating Ca2+ cycling proteins and contractility in chronic ethanol exposed cardiocytes. Parallel measures of IC and sarcomere/cellular contractions were assessed (Ionoptix) with the expression level (western blot) of Ca2+ handling proteins (sarcoplasmic reticulum calcium ATPase(SERCA2a), phospholamban(PLN), Na+‐Ca2+ exchanger (NCX) and L‐type Ca2+ channels(LTCC)) from control, low (LA: 0.02%), and high (HA: 0.45%) alcoholic rat hearts (4 months on Lieber DiCarli liquid diet), with and without Ad.EGFP and Ad.Akt transfection. Our results show an inotropically damaging increase in IC with HA but not with LA. In parallel, NCX protein expression is diminished in HA whereas that of LTCCs is increased. In addition, SERCA2a levels are increased in LA and decreased in HA. Upon Ad.Akt transfection SERCA2a levels increased in HA. Protein levels of phosphorylated PLN also increased in LA and decreased in HA hearts. This suggests that chronic ethanol elevates IC to harmful levels through cytoplasmic trapping via NCX which is exacerbated by reduced SERCA2a through PLN in an Akt‐dependent manner.Grant Funding Source: Supported by NIH/NIAAA/1R15AAA019816‐01A1 and 2G12 RR003048
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.
