Howard A. Rockman, MD

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Services

• General and Consultative Heart Care

Chief

Department / Division:
Medicine / Cardiovascular Medicine

Address:
DUMC 3104
Durham, NC 27710

Appointment Telephone:
(919) 681-5816

Office Telephone:
(919) 668-2520

Fax Telephone:
(919) 668-2524

• M.D., McGill University, Montreal, Canada, 1983

• Internal Medicine, Montreal General Hospital, McGill University, Canada, 1984-1987
• Cardiology, University of California at San Diego, 1987-1989

• Cardiology Research, University of California at San Diego, 1989-1991

Clinical Interests:
General cardiology, heart failure

Research Interests:
Rockman Lab:  Molecular Mechanisms of Hypertrophy and Heart Failure

Overall Research Direction:  The major focus of this laboratory is to understand the molecular mechanisms of hypertrophy and heart failure.  My laboratory uses a strategy that combines state of the art molecular techniques to generate transgenic and gene targeted mouse models, combined with sophisticated physiologic measures of in vivo cardiac function.  In this manner, candidate molecules are either selectively overexpressed in the mouse heart or ablated by homologous recombination, which is followed by an in-depth analysis of the physiological phenotype.  To model human cardiac disease, we have created several models of cardiac overload in the mouse using both microsurgical techniques and genetic models of cardiac dysfunction.

Areas of Research
1) Signaling:  G protein-coupled receptor signaling in hypertrophy and heart failure focusing on the interaction of phosphoinositide-3 kinase with b-adrenergic receptors.

2) Identification of Genetic Modifiers of Cardiomyopathy:  Quantitative trait loci mapping of gene modifiers and N-ethyl-N-nitrosourea (ENU) mutagenesis that alter the heart failure phenotype using disease-sensitized mouse models.

3) Molecular physiology:  In depth physiological analysis of cardiac function in genetically altered mice to understand the role of G protein-coupled receptor signaling pathways on the development of heart failure in vivo.

4) Deletion screens in Drosophila:  To detect novel genes important for cardiac function in the adult fly .

Representative Publications:
Rockman HA, Koch WJ, Lefkowitz RJ. Seven-transmembrane-spanning receptors and heart function. Nature. 2002 Jan 10;415(6868):206-12. (2002) Abstract

Nienaber JJ, Tachibana H, Naga Prasad SV, Esposito G, Wu D, Mao L, Rockman HA. Inhibition of receptor-localized PI3K preserves cardiac beta-adrenergic receptor function and ameliorates pressure overload heart failure. J Clin Invest. 2003 Oct;112(7):1067-79. (2003) Abstract

Naga Prasad SV, Jayatilleke A, Madamanchi A, Rockman HA. Protein kinase activity of phosphoinositide 3-kinase regulates beta-adrenergic receptor endocytosis. Nat Cell Biol. 2005 Aug;7(8):785-96. (2005) Abstract

Perrino C, Naga Prasad SV, Schroder JN, Hata JA, Milano C, Rockman HA. Restoration of beta-adrenergic receptor signaling and contractile function in heart failure by disruption of the betaARK1/phosphoinositide 3-kinase complex. Circulation. 2005 May 24;111(20):2579-87. (2005) Abstract

Perrino C, Naga Prasad SV, Mao L, Noma T, Yan Z, Kim HS, Smithies O, Rockman HA. Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction. J Clin Invest. 2006 Jun;116(6):1547-60. (2006) Abstract

Wolf MJ, Amrein H, Izatt JA, Choma MA, Reedy MC, Rockman HA. Drosophila as a model for the identification of genes causing adult human heart disease. Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1394-9. (2006) Abstract

Volovyk ZM, Wolf MJ, Prasad SV, Rockman HA. Agonist-stimulated beta-adrenergic receptor internalization requires dynamic cytoskeletal actin turnover. J Biol Chem. 2006 Apr 7;281(14):9773-80. (2006) Abstract