Abstract

OF WORK: Core B ? Comprehensive Mouse Physiology and Phenotyping Comprehensive mouse physiology and mouse phenotyping including surgical models of pressure overload to induce cardiac hypertrophy and heart failure. The PI's laboratory has considerable expertise in a wide-range of methodologies for the phenotyping of mice and will provide Core service to members of the PPG. The PI has also been involved in the development of numerous genetic and surgical models of heart failure. For example, microsurgical procedures and hemodynamic evaluation of pressure overload cardiac hypertrophy induced through transverse aortic constriction was developed by the PI, and is now considered a routine procedure in many labs around the world. Transthoracic 2D guided M-mode echocardiography, hemodynamic and contractile function by pressure-volume loops and stress strain analyses in mice are standard procedures, many which were developed in the PI's laboratory. Exercise training by both swimming and wheel running for mice are methods currently being used.

Public Health Relevance

Core B ? Comprehensive Mouse Physiology and Phenotyping To elucidate the molecular intersection of novel adrenergic receptor signaling pathways involved in the physiological and pathophysiological growth of the heart with a particular focus on identifying new molecular therapeutic targets and strategies in heart failure.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL075443-14
Application #
9475649
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Program Officer
Adhikari, Bishow B
Project Start
Project End
Budget Start
2018-06-01
Budget End
2019-05-31
Support Year
14
Fiscal Year
2018
Total Cost
Indirect Cost

  Institution

Name
Duke University
Department
Type
DUNS #
044387793
City
Durham
State
NC
Country
United States
Zip Code
27705

  Publications

Kim, Jihee; Grotegut, Chad A; Wisler, James W et al. (2018) ?-arrestin 1 regulates ?2-adrenergic receptor-mediated skeletal muscle hypertrophy and contractility. Skelet Muscle 8:39
Zhou, Hua-Lin; Stomberski, Colin T; Stamler, Jonathan S (2018) Cross Talk Between S-Nitrosylation and Phosphorylation Involving Kinases and Nitrosylases. Circ Res 122:1485-1487
de Lucia, Claudio; Gambino, Giuseppina; Petraglia, Laura et al. (2018) Long-Term Caloric Restriction Improves Cardiac Function, Remodeling, Adrenergic Responsiveness, and Sympathetic Innervation in a Model of Postischemic Heart Failure. Circ Heart Fail 11:e004153
Grisanti, Laurel A; Schumacher, Sarah M; Tilley, Douglas G et al. (2018) Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease. JACC Basic Transl Sci 3:550-562
de Lucia, Claudio; Eguchi, Akito; Koch, Walter J (2018) New Insights in Cardiac ?-Adrenergic Signaling During Heart Failure and Aging. Front Pharmacol 9:904
Wang, Jialu; Hanada, Kenji; Gareri, Clarice et al. (2018) Mechanoactivation of the angiotensin II type 1 receptor induces ?-arrestin-biased signaling through G?i coupling. J Cell Biochem 119:3586-3597
Hayashi, Hiroki; Hess, Douglas T; Zhang, Rongli et al. (2018) S-Nitrosylation of ?-Arrestins Biases Receptor Signaling and Confers Ligand Independence. Mol Cell 70:473-487.e6
Rizza, Salvatore; Cardaci, Simone; Montagna, Costanza et al. (2018) S-nitrosylation drives cell senescence and aging in mammals by controlling mitochondrial dynamics and mitophagy. Proc Natl Acad Sci U S A 115:E3388-E3397
Cannavo, Alessandro; Koch, Walter J (2018) GRK2 as negative modulator of NO bioavailability: Implications for cardiovascular disease. Cell Signal 41:33-40
Wang, Jialu; Gareri, Clarice; Rockman, Howard A (2018) G-Protein-Coupled Receptors in Heart Disease. Circ Res 123:716-735

Showing the most recent 10 out of 167 publications