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Akt/PI3K signaling sustains the acute alcoholic effects in isolated rat cardicytes
Author(s) -
Umoh Nsini Alease,
Walker Robin K.,
Jeffress Miara,
Cousins Valerie,
AlRubaiee Mustafa,
Haddad Georges E.
Publication year - 2013
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.27.1_supplement.1197.4
Subject(s) - protein kinase b , pi3k/akt/mtor pathway , medicine , apoptosis , alcoholic cardiomyopathy , endocrinology , viability assay , cancer research , pharmacology , heart failure , cardiomyopathy , chemistry , biochemistry
Cardiovascular diseases are the leading causes of increased mortality and morbidity rates. High alcohol consumption has been shown to negatively impact the heart function into having reduced contractility with cardiomyopathy. However, low alcohol consumption is shown to have beneficial effects on the heart. Prior studies in our lab have linked the Akt/PI3K pathway to cardiac dysfunction during eccentric hypertrophy. In this study, we investigate the role of Akt activity (western blot) that contributes to changes in cardiac contraction (Ionoptix), cell survival (Cell Viability Assay), and caspase activity (caspase 3/7 assay), associated with low (5mM) and high (100mM) alcohol consumption. Our results demonstrate that Akt overexpression increased cardiocyte survival during low alcohol exposure. However, the effects of Akt are diminished with high alcohol exposure. Low alcohol also decreased caspase activity and increased cellular and sarcomere contraction. Knockout of the Akt gene negated the above effects of Akt, and therefore decreased cell survival, and increased caspase activity. Our data suggests that Akt signaling plays an important role in supporting the beneficial effects of low alcohol which is diminished with high alcohol exposure having detrimental effects on cardiocyte function. This work was supported in part by grants NIH/NIAAA/1R15AAA019816–01A1, and 2G12 RR003048 RCMI/NCRR/NIH.