This core unit will be available to all investigators on the Program Project and will provide physiologic and morphologic characterization of cardiovascular phenotypes, using miniaturized hemodynamic and imaging methods along with microsurgical techniques for in vivo physiological studies in mice. The goals of this core facility are to: 1) provide detailed phenotyping of genetically engineered murine models using imaging to assess functional cardiac morphology, primarily transthoracic echocardiography and contrast angiocardiography, and a variety of hemodynamic techniques for evaluating the physiologic status of the heart; 2) apply microsurgical methods in mice for inducing pressure overload on either the left or right ventricle, or to produce myocardial infarction, in order to induce ventricular remodeling with hypertrophy or heart failure; and 3) extend to mice high efficiency in vivo cardiac gene transfer methods recently developed in hamsters and rats.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
2P01HL046345-11
Application #
6651376
Study Section
Project Start
2002-08-25
Project End
2007-07-31
Budget Start
Budget End
Support Year
11
Fiscal Year
2002
Total Cost
$106,600
Indirect Cost
Name
University of California San Diego
Department
Type
DUNS #
077758407
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Dewan, Sukriti; McCabe, Kimberly J; Regnier, Michael et al. (2016) Molecular Effects of cTnC DCM Mutations on Calcium Sensitivity and Myofilament Activation-An Integrated Multiscale Modeling Study. J Phys Chem B 120:8264-75
Peter, Angela K; Bradford, William H; Dalton, Nancy D et al. (2016) Increased Echogenicity and Radiodense Foci on Echocardiogram and MicroCT in Murine Myocarditis. PLoS One 11:e0159971
Sheikh, Farah; Lyon, Robert C; Chen, Ju (2015) Functions of myosin light chain-2 (MYL2) in cardiac muscle and disease. Gene 569:14-20
Israeli-Rosenberg, Sharon; Chen, Chao; Li, Ruixia et al. (2015) Caveolin modulates integrin function and mechanical activation in the cardiomyocyte. FASEB J 29:374-84
Stroud, Matthew J; Banerjee, Indroneal; Veevers, Jennifer et al. (2014) Linker of nucleoskeleton and cytoskeleton complex proteins in cardiac structure, function, and disease. Circ Res 114:538-48
Zemljic-Harpf, Alice E; Godoy, Joseph C; Platoshyn, Oleksandr et al. (2014) Vinculin directly binds zonula occludens-1 and is essential for stabilizing connexin-43-containing gap junctions in cardiac myocytes. J Cell Sci 127:1104-16
Lyon, Robert C; Mezzano, Valeria; Wright, Adam T et al. (2014) Connexin defects underlie arrhythmogenic right ventricular cardiomyopathy in a novel mouse model. Hum Mol Genet 23:1134-50
Pfeiffer, E R; Wright, A T; Edwards, A G et al. (2014) Caveolae in ventricular myocytes are required for stretch-dependent conduction slowing. J Mol Cell Cardiol 76:265-74
Bang, Marie-Louise; Gu, Yusu; Dalton, Nancy D et al. (2014) The muscle ankyrin repeat proteins CARP, Ankrd2, and DARP are not essential for normal cardiac development and function at basal conditions and in response to pressure overload. PLoS One 9:e93638
Israeli-Rosenberg, Sharon; Manso, Ana Maria; Okada, Hideshi et al. (2014) Integrins and integrin-associated proteins in the cardiac myocyte. Circ Res 114:572-586

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