This Core will provide high-fidelity measures of cardiac physiology for the various mouse lines described in the 3 Projects and provide models of cardiac injury for all Projects to study. Specifically, this Core Unit will be responsible for providing 1) mouse models of cardiac hypertrophy and ischemic injury where both models can lead to heart failure (HF), 2) complete and comprehensive cardiovascular physiology measurements (phenotyping) of all mouse models detailed through the PPG application, and 3) cardiac viral-mediated gene delivery. Surgical mouse models include coronary artery occlusion models for ischemia/reperfusion (l/R) injury or complete coronary artery ligation producing a myocardial infarction (Ml). Also, transverse aortic constriction (TAC) for models of hypertrophy and HF will be handled in this Core. The Core will also help investigators with surgical implantation of AzIet mini-osmotic pumps for chronic drug delivery. Further, cardiac viral-mediated gene delivery can be done either though IV injection or more invasively directly to the heart as seen in this application. Comprehensive mouse cardiovascular physiological phenotyping includes in-depth assessment of murine in vivo cardiac function via echocardiography and hemodynamic measurements via Millar catheterization. Further, this Core will assess conscious blood pressure and electric cardiogram (ECG) using telemetry. This Core will be utilized by all Projects and will continue to be instrumental in providing reproducible and high-quality mouse models of cardiac injury and physiological cardiovascular phenotyping.

Public Health Relevance

Mouse models of cardiac injury have been key tools to delineate novel mechanisms of heart failure development and to also test unique therapeutic strategies for repair of the failing heart. This Core is instrumental to the success of all Projects within this PPG and will continue to provide significant support in animal model and cardiovascular phenotyping.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Research Program Projects (P01)
Project #
Application #
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Temple University
United States
Zip Code
Ahmad, Firdos; Lal, Hind; Zhou, Jibin et al. (2014) Cardiomyocyte-specific deletion of Gsk3? mitigates post-myocardial infarction remodeling, contractile dysfunction, and heart failure. J Am Coll Cardiol 64:696-706
Bathgate-Siryk, Ashley; Dabul, Samalia; Pandya, Krunal et al. (2014) Negative impact of *-arrestin-1 on post-myocardial infarction heart failure via cardiac and adrenal-dependent neurohormonal mechanisms. Hypertension 63:404-12
Scimia, Maria Cecilia; Blass, Benjamin E; Koch, Walter J (2014) Apelin receptor: its responsiveness to stretch mechanisms and its potential for cardiovascular therapy. Expert Rev Cardiovasc Ther 12:733-41
Lal, Hind; Ahmad, Firdos; Parikh, Shan et al. (2014) Troponin I-interacting protein kinase: a novel cardiac-specific kinase, emerging as a molecular target for the treatment of cardiac disease. Circ J 78:1514-9
Hullmann, Jonathan E; Grisanti, Laurel A; Makarewich, Catherine A et al. (2014) GRK5-mediated exacerbation of pathological cardiac hypertrophy involves facilitation of nuclear NFAT activity. Circ Res 115:976-85
Miller, Barbara A; Hoffman, Nicholas E; Merali, Salim et al. (2014) TRPM2 channels protect against cardiac ischemia-reperfusion injury: role of mitochondria. J Biol Chem 289:7615-29
Tilley, Douglas G; Zhu, Weizhong; Myers, Valerie D et al. (2014) ?-adrenergic receptor-mediated cardiac contractility is inhibited via vasopressin type 1A-receptor-dependent signaling. Circulation 130:1800-11
Feldman, Arthur M; Begay, Rene L; Knezevic, Tijana et al. (2014) Decreased levels of BAG3 in a family with a rare variant and in idiopathic dilated cardiomyopathy. J Cell Physiol 229:1697-702
Scimia, Maria C; Gumpert, Anna M; Koch, Walter J (2014) Cardiovascular gene therapy for myocardial infarction. Expert Opin Biol Ther 14:183-95
Wang, JuFang; Song, Jianliang; Gao, Erhe et al. (2014) Induced overexpression of phospholemman S68E mutant improves cardiac contractility and mortality after ischemia-reperfusion. Am J Physiol Heart Circ Physiol 306:H1066-77

Showing the most recent 10 out of 81 publications