Jeannette Vasquez-Vivar, PhD
Associate Director, Redox Biology Program
Education & Experience
- Universidad de Concepción Chile (Chile), BS, Biochemistry (1995)
- Universidade de São Paulo (Brazil), PhD, Biochemistry (1986)
- Instituto de Química, Universidade de São Paulo (Brazil), Postdoctoral Fellow in Biochemistry (1993-1996)
- Medical College of Wisconsin (Milwaukee, WI), Research Fellow in Pathology (1996-1998)
As a postdoctoral fellow, I investigated kinetics and mechanisms of free radical formation from reactions involving peroxynitrite and biomolecules, and later I discovered the role of tetrahydrobiopterin in the regulation of superoxide release from nitric oxide synthase. In 1998, I became a faculty member in the Department of Pathology at MCW, studying the endothelial nitric oxide synthase uncoupling in endothelial dysfunction. In 2001, I joined the faculty of the Department of Biophysics at MCW, where I continue my work on redox mechanisms of cardiovascular and fetal brain dysfunction.
My lab investigates cell-specific redox mechanisms disrupting normal cellular homeostasis. We focus on three different systems: fetal brain, heart, and endothelial cells. My research is supported by the National Institutes of Health.
Our project dealing with the fetal brain is supported by our discovery that a developmentally low tetrahydrobiopterin (BH4) cofactor in the fetal brain increases hypoxia-ischemia injury in specific brain regions and worsens motor disabilities in newborns. Our working hypothesis is that development of motor deficits can be explained by a two-hit model where transient low tetrahydrobiopterin represents an important vulnerability state of immature fetal brain neurons. In collaboration with the group of Dr. Tan (Wayne State University), we are testing the idea that BH4 is a critical neuronal developmental factor.
Our BH4 effects in cardiovascular health project examines the relationship between endothelial dysfunction and eNOS uncoupling in an animal model of atherosclerosis. While eNOS dysfunction is believed to be an important element promoting vascular dysfunction, it is yet unclear whether eNOS uncoupling controls a state of critical oxidant stress to promote disease. In this project we are examining the impact of BH4 in redox that could further support therapeutic effects in hypercholesterolemia. A second approach is to understand the role of BH4 in cardiomyocyte redox changes that could link BH4 deficiency with loss of function as could occur in heart failure.
- Karhikeyan Thirugnanam, Postdoctoral Fellow