Stephen Black

Research Focus Group Membership: 
Research Focus Group 2
  • PhD: University of Edinburgh, Scotland, Molecular Pharmacology, 1990
  • MD: University of Edinburgh, Scotland, 1982
  • BS: University of Edinburgh, Scotland, Molecular Biology, 1986
College Affiliations: 

College of Pharmacy
College of Medicine

Research Interests: 

Work in Dr. Stephen Black’s laboratory is focused on understanding the mechanisms underlying the development of the endothelial dysfunction that precedes the development of PH (Pulmonary Hypertension), the role of reactive oxygen species in this process, and understanding how decreased NO signaling leads to the pulmonary vascular remodeling that is associated with more advanced disease.

Environmental Health Research & Expertise: 

My laboratory is an integrated cardiovascular laboratory studying vascular function with a focus on understanding how reactive nitrogen species (RNS) generation alters mitochondrial and endothelial function both in vitro and in vivo. Our expertise allows us to use of state of the art mass spectroscopy techniques in conjunction with cellular techniques to elucidate how post-translational modifications alter protein structure-function relationships and to elucidate pathways how RNS signaling is regulated in endothelial cells in both physiologic and pathologic situations. Further, we also have the expertise to carry these studies into clinically relevant animal models of endothelial dysfunction both to confirm our cell culture studies and, through directed interventions, to modulate these signaling pathways to determine effects on endothelial function in the intact animal. Further, though collaboration with clinician investigators we are now expanding our studies into humans. My laboratory is unique in its ability to cover such as breadth of investigations. We have several major projects currently extramurally funded or are pending funding. 1) Perinatal regulation of endothelial NOS; 2) Role of altered carnitine metabolism in perinatal endothelial dysfunction; 3) ROS in pulmonary hypertension; 4) Endothelial barrier protection and repair in acute lung injury.