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Pressure‐Overload Hypertrophy of the Developing Heart Reveals Activation of Divergent Gene and Protein Pathways in the Left and Right Ventricular Myocardium
Author(s) -
Friehs Ingeborg,
Cowan Douglas B,
Choi YeongHoon,
Black Kendra M,
Barnett Reanne,
Del Nido Pedro J,
Levitsky Sidney,
McCully James D
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.386.7
Subject(s) - pressure overload , muscle hypertrophy , biology , medicine , heart failure , mitochondrion , gene expression , phosphorylation , pulmonary artery banding , microarray , oxidative phosphorylation , endocrinology , pulmonary artery , microbiology and biotechnology , gene , cardiac hypertrophy , biochemistry
Right (RV) and left ventricular (LV) myocardium differ in their pathophysiological response to pressure‐overload hypertrophy (POH). Herein we use microarray and proteomic analyses to identify pathways modulated in LV‐ and RV‐ POH. Newborn New Zealand White rabbits underwent banding of the descending thoracic aorta (LV‐AOB; n=6) or banding of the pulmonary artery (RV‐PAB; n=6). Controls (SC; n=6 each) were sham‐manipulated. Following 4 (LV‐AOB) and 6 weeks (RV‐PAB) recovery, the hearts were removed and matched RNA and protein samples were isolated for microarray and proteomic analysis as compared to SC. Our results demonstrate there was increased transcript expression levels for mitochondria energy pathways, actin, hypoxia, calcium and protein kinase‐A signalling and increased protein expression levels for cellular macromolecular complex assembly and oxidative phosphorylation in LV‐AOB. In RV‐PAB there was increased transcript expression levels for cardiac oxidative phosphorylation and increased protein expression levels for cardiac muscle tissue development and calcium handling. Our results demonstrate that the mitochondrion plays an important but varied role to support divergent compensatory pathways in LV‐ and RV‐POH. These data provide new insight into the biological basis of LV‐ and RV‐POH during compensation and identify novel therapeutic pathways for intervention prior to failure.