This is a revision of an application submitted by the Physiology Department and the Cardiovascular Research Center at Temple University School of Medicine The purpose of our program is to provide a broad based multidisciplinary training experience for predoctoral fellows and summer medical students in the area of integrative cardiovascular pathophysiology (ICVP). ICVP faculty reside in the Physiology, Anatomy and Cell Biology, Biochemistry, and Microbiology. Most of these faculty members are housed together in laboratory space within a newly developed Cardiovascular Research Center. Our investigators have overlapping interests in electrical and mechanical properties of normal and diseased cardiac myocytes, and the factors that promote recovery of damaged myocardium, including cardiac stem cells. Newly recruited and established CVRC faculty also study the cellular and molecular properties of fibroblasts, myocytes, smooth muscle and blood cells as well as the control and regulation of the extracellular matrix of the heart and blood vessels. All investigators have a portion of their research related to the role of their favorite molecule, signaling pathway or cell type in a major cardiovascular disease, including hypertension, atheroscerlosis, vascular injury, myocardial infarction and congestive heart failure. Graduate students will receive broad training in human physiology and pathophysiology, complemented by advanced training in cellular and molecular biology and the appropriate use of animal models of human cardiovascular disease. Ph.D. student research projects will have basic and translational components. The student will be expected to ask questions that go beyond a single molecule and address questions within the context of cardiovascular disease models. Different portions of these projects will be performed in the laboratories of different investigators, ensuring that students are exposed to different scientific approaches. All students and fellows will be involved in activities to enhance their grant and manuscript writing and oral communication skills. Group mentoring by junior and senior faculty will ensure trainees are well qualified to assume positions as leading investigators able to rapidly translate new knowledge into clinical practice. The goal is to graduate new Ph.D. that are able to compete for top rated postdoctoral positions, to fulfill the need for new investigators to discover mechanisms of human disease.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
5T32HL091804-02
Application #
7681147
Study Section
NHLBI Institutional Training Mechanism Review Committee (NITM)
Program Officer
Carlson, Drew E
Project Start
2008-09-01
Project End
2013-08-31
Budget Start
2009-09-01
Budget End
2010-08-31
Support Year
2
Fiscal Year
2009
Total Cost
$206,638
Indirect Cost
Name
Temple University
Department
Physiology
Type
Schools of Medicine
DUNS #
057123192
City
Philadelphia
State
PA
Country
United States
Zip Code
19122
Harper, Shavonn C; Brack, Andrew; MacDonnell, Scott et al. (2016) Is Growth Differentiation Factor 11 a Realistic Therapeutic for Aging-Dependent Muscle Defects? Circ Res 118:1143-50; discussion 1150
Wallner, Markus; Duran, Jason M; Mohsin, Sadia et al. (2016) Acute Catecholamine Exposure Causes Reversible Myocyte Injury Without Cardiac Regeneration. Circ Res 119:865-79
Hullmann, Jonathan; Traynham, Christopher J; Coleman, Ryan C et al. (2016) The expanding GRK interactome: Implications in cardiovascular disease and potential for therapeutic development. Pharmacol Res 110:52-64
Grisanti, Laurel A; Traynham, Christopher J; Repas, Ashley A et al. (2016) ?2-Adrenergic receptor-dependent chemokine receptor 2 expression regulates leukocyte recruitment to the heart following acute injury. Proc Natl Acad Sci U S A 113:15126-15131
Traynham, Christopher J; Cannavo, Alessandro; Zhou, Yan et al. (2015) Differential Role of G Protein-Coupled Receptor Kinase 5 in Physiological Versus Pathological Cardiac Hypertrophy. Circ Res 117:1001-12
Smith, Shavonn C; Zhang, Xiaoxiao; Zhang, Xiaoying et al. (2015) GDF11 does not rescue aging-related pathological hypertrophy. Circ Res 117:926-32
Trappanese, Danielle M; Liu, Yuchuan; McCormick, Ryan C et al. (2015) Chronic ?1-adrenergic blockade enhances myocardial ?3-adrenergic coupling with nitric oxide-cGMP signaling in a canine model of chronic volume overload: new insight into mechanisms of cardiac benefit with selective ?1-blocker therapy. Basic Res Cardiol 110:456
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
Ellison, Stephen; Gabunia, Khatuna; Richards, James M et al. (2014) IL-19 reduces ligation-mediated neointimal hyperplasia by reducing vascular smooth muscle cell activation. Am J Pathol 184:2134-43
Duran, Jason M; Makarewich, Catherine A; Trappanese, Danielle et al. (2014) Sorafenib cardiotoxicity increases mortality after myocardial infarction. Circ Res 114:1700-1712

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