Approaches
to Myocardial Injury Protection
Molecular Mechanisms of Cardiac Hypertrophy & Heart Failure
Cardiovascular
disease is a primary cause of death in the United States. Understanding
the pathogenesis and mechanisms that lead to heart disease may
result in novel therapies to reduce myocardial damage caused by
a heart attack and alleviate cardiac dysfunction that accompanies
hypertrophy and failure. The overall directions of my research
program are two-fold: 1) identify and characterize signaling events
involved in protecting the myocardium from ischemic injury and
cell death following myocardial infarction (i.e., heart attack)
and 2) determine the mechanisms by which cardiac hypertrophy and
heart failure occur following myocardial infarction or hemodynamic
load (high blood pressure or volume overload).
In
vivo and in vitro physiological approaches are utilized in my
lab to elucidate the contribution of the opioid and growth factor
receptor systems to cardiac pathophysiology. We routinely employ
echocardiography, work-performing and Langendorff whole heart
preparations, in vivo hemodynamic measurements, and isolation
and analysis of cardiomyocytes. In addition, a number of surgical
techniques (aortic banding, coronary artery ligation, catheterizations)
are used in my laboratory. Throughout these studies, pharmacological,
histological, biochemical, and state-of-the art molecular biology
assays are employed, and include Northern blot and quantitative
real-time PCR analysis for mRNA expression, and protein analysis
via Western blot, ELISA and immunostaining. Genomic and proteomic
tools, including DNA microarrays, are implemented in the lab to
further characterize or identify known and novel mechanism(s)
of opioid- and growth factor-mediated cardiovascular physiology
and pathology.
Ongoing
Research Projects:
1)
Fibroblast Growth Factor 2 (FGF2) and cardioprotection
2) Opioidergic systems and cardiac hypertrophy and heart failure
Publications (PubMed)
