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RESEARCH FACULTY

Marcelo Bonini, PhD — research focuses on contributing to the understanding of the role of enzyme components of the nitric oxide signaling cascade and oxidative stress in the regulation of agonist-dependent vasodilation, and the role of signal transduction pathways involved in the hypotensive effects of nitroglycerin. They use diverse biochemical and biophysical techniques which include immunochemical-based approaches, confocal and electron microscopy, electron paramagnetic resonance, HPLC, PCR, genetically modified organisms (cells and knockout animals), fluorescence and UV/Visible spectrometry to identify the role of nitric oxide synthases, phosphatase and tensin homolog deleted in chromosome 10 (PTEN), PI3k and Akt/PKB in the biological effects elicited by nitroglycerin and agonist-dependent vasodilation under a variety of physiological and inflammatory conditions.


Tohru Fukai, PhD — Oxidative stress has been implicated in the pathogenesis of many cardiovascular diseases, including hypercholesterolemia, atherosclerosis, hypertension, diabetes, and heart failure.The major focus of Dr. Fukai’s research is a role of antioxidant enzyme, such as extracellular superoxide dismutase (ecSOD) its new regulator, copper transport proteins in cardiovascular disease. ecSOD is one of the major copper containing antioxidant enzymes in the vasculature, and plays an important role in regulating blood pressure, neovascularization, and endothelial function by preventing oxidative inactivation of NO.Most recently, his laboratory demonstrated that copper transport system is not only a key regulator of ecSOD activity and expression, but also a fundamental regulator of growth factor signaling. Thus, the long-term goal of his lab is to determine the role of copper homeostasis and copper transport system for ecSOD as well as to define their functional relationships in oxidative stress-dependent cardiovascular disease.

Beata M. Wolska, Ph.D. — My laboratory is interested in the membrane and myofilament control of cardiacfunction both in physiological and pathological conditions such as HCM, DCM and heart failure (HF). We focus on the role of myofilaments, Ca2+ delivery to and from myofilaments, signaling pathways and how they interact and alter each other. Our recent work in animal models has attempted to rescue HCM and DCM via modifications at the myofilament level or through altering Ca2+ homeostasis by targeting Ca2+-handling proteins. The ultimate goal of our studies using integrative approach is to obtain unique insight into the pathophysiology of HCM, DCM and HF and development of individual-based therapies that could potentially replace ormodify current treatments.