Gregory B Waypa

Calculated based on number of publications stored in Pure and citations from Scopus
Calculated based on number of publications stored in Pure and citations from Scopus
Calculated based on number of publications stored in Pure and citations from Scopus

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Personal profile

Research Interests

Gregory B. Waypa, Ph.D. received his B.S. in Biomedical Engineering Sciences from the University of California, San Diego in 1991. He then enrolled as a graduate student at Albany Medical College in Albany, New York, where, under Fred L. Minnear, Ph.D., he studied increased pulmonary vascular permeability associated acute respiratory distress syndrome (ARDS) and explored the possibility of using cAMP-enhancing agents as a possible therapy for the disease. Dr. Waypa received his M.S., and later his Ph.D., in Physiology and Cell Biology from Albany Medical College in 1997 and 1998, respectively. From 1998 to 2002, Dr. Waypa was a postdoctoral fellow with Paul T. Schumacker, Ph.D. at The University of Chicago. In 2002, Dr. Waypa received an appointment from The University of Chicago as a Research Associate (Assistant Professor) where he continued to work with Dr. Schumacker. In 2004, Dr. Waypa received an appointment from Northwestern University as a Research Assistant Professor where he is continuing his collaboration with Dr. Schumacker. In 2015, Dr. Waypa was promoted to Research Associate Professor in the Department of Pediatrics and Neonatology. Currently, Dr. Waypa is studying hypoxic pulmonary vasoconstriction (HPV), which is a physiological response to low alveolar oxygen tension and, in cases where a small percentage of the lung alveoli are hypoxic, HPV improves lung gas exchange by redistributing blood flow away from those areas toward regions with better oxygenation. Key to this research is understanding the mechanism of O2 sensing by the pulmonary vasculature and how this results in the generation of the HPV response.


Currently, I am studying acute and chronic hypoxic pulmonary vasoconstriction (HPV), a physiological response where pulmonary arteries constrict in response to alveolar hypoxia. During chronic alveolar hypoxia, this pulmonary vasoconstriction can result in the development of pulmonary hypertension, right ventricular hypertrophy, cor pulmonale, and death. An important unresolved question in this field relates to the underlying mechanism by which the vascular cells detect a decrease in oxygen tension and translate that into a signal that triggers the functional response. I have been collaborating with Dr. Schumacker in testing the hypothesis that the mitochondria function as O2 sensors by initiating a reactive oxygen species signaling pathway that triggers the HPV response. I have focused my efforts on the use of imaging methodology to address this question, using ratiometric, genetically encoded fluorescent sensors (roGFP) targeted to subcellular compartments including the cytosol, mitochondrial matrix, and intermembrane space of mitochondria. I have also used genetically encoded, ratiometric calcium sensors targeted to the cytosol or the mitochondrial matrix to assess calcium signaling using imaging techniques. I am currently extending our imaging technology by engineering transgenic mice expressing cell-specific, targeted roGFP. By employing these mice, we will be able to induce the expression of the roGFP in endothelial cells or in smooth muscle cells. In addition, I’ve begun to measure changes in pulmonary hemodynamics in mice challenged with acute and chronic hypoxia. We will use these approaches to assess changes in pulmonary hemodynamics in whole mice and redox and calcium signaling in vascular cells in precision cut lung slices as well as in intact lungs of mice subjected to acute hypoxia, chronic hypoxia, or control conditions.

Education/Academic qualification

PhD, Albany Medical College

… → 1998

Research interests keywords

  • Angiogenesis
  • Apoptosis
  • Bioengineering
  • Cell Biology
  • Circulation
  • Molecular Biology
  • Physiology
  • Signal Transduction


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