Premium
Mitochondrial proliferation is not affected by inhibition of the intracellular renin‐angiotensin system
Author(s) -
Ruiz Louis,
Rullan Rebecca Parodi,
Javadov Sabzali
Publication year - 2012
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.26.1_supplement.lb604
Subject(s) - renin–angiotensin system , losartan , angiotensin ii , intracellular , aliskiren , muscle hypertrophy , medicine , endocrinology , cell growth , chemistry , microbiology and biotechnology , cardioprotection , mapk/erk pathway , phosphorylation , biology , receptor , biochemistry , ischemia , blood pressure
Inhibition of the renin‐angiotensin system (RAS) has shown to exert cardioprotection against hypertrophy and heart failure independent of their anti‐hypertensive effects. However, molecular mechanisms underlying the benefits of RAS inhibition mediated through the intracellular RAS system on cardiac cells remain to be elucidated. We examined the contribution of mitochondrial proliferation to the anti‐hypertrophic actions of the RAS inhibitors, losartan and aliskiren. An in vitro model of hypertrophy was induced on H9c2 myoblastic cells with angiotensin II (Ang II). Results demonstrated that hypertrophy‐induced stimulation of cell signaling was associated with an increase in cell surface area and ERK1/2 MAPK phosphorylation by 19% (p <0.05) and 39% (p <0.05), respectively. Treatment with RAS inhibitors prevented hypertrophy as evidenced by normalization of AngII effects. Fluorescence activated cell sorting (FACS) analysis revealed reduced mitochondrial proliferation in AngII‐treated cells which was not prevented by RAS inhibition. Conclusively, this study demonstrates that inhibition of the RAS attenuates AngII‐induced hypertrophy in H9c2 cells that is not associated with mitochondrial proliferation.