Redox Biology Program

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Jeannette M. Vasquez Vivar, PhD

Phone:  414-955-8095 
Fax:      414-955-6512
Email:   jvvivar@mcw.edu

Vasquez Vivar Laboratory

The general interest of the laboratory is to investigate cell-specific redox mechanisms disrupting normal cellular homeostasis. The research group has focused on three different systems: fetal brain, heart and endothelial cells.

Endothelial Cells

The endothelial 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 the researchers are examining whether eNOS uncoupling is necessary to reach a state of critical oxidative stress causing significant changes in the vascular wall and testing its reversibility by BH4 therapies.

 

   

The Heart Project

The heart project investigates the influence of mitochondrial DNA variants in cardiac remodeling. The research team has shown that hearts from conplastic rat strains (i.e., animals with identical nuclear but different mitochondrial genome) expressing mtDNA variant (mtFHH) leading to low complex I activity and bioenergetic impairments, undergo cardiac remodeling. The group hypothesizes that the decreased OXPHOS activity translates into NAD+-regulated redox signaling from mitochondria to nuclear genome capable of promoting cardiac adaptive growth responses.

 

   

 

The Fetal Brain Project

The project dealing with fetal brain is supported by the investigators’ discovery that developmentally low tetrahydrobiopterin (BH4) cofactor in the fetal brain increases hypoxia-ischemia injury in specific brain regions and worsens motor disabilities in newborns. The research group’s 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.

 

   

 

 

 

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