Current Fellows

Katherine Wood, PhD


Dr. Katherine Wood completed her undergraduate studies in Political Science at the University of Louisiana at Lafayette. She went on to get her PhD in Molecular and Cellular Physiology from the Louisiana State University of Health Sciences Center-Shreveport, where her research work in Dr. Neil Granger’s group focused on elucidating the contributions of the circulating blood cell and vascular endothelial cell compartments to P-selectin, NADPH oxidase and uncoupled endothelial cell nitric oxide synthase (eNOS) in the cerebral vasculopathy of sickle cell disease (SCD). Early postdoctoral research work at the NIH, under the mentorship of Drs. Mark Gladwin and Gregory Kato primarily focused on identifying important contributions of red blood cell eNOS to physiological blood pressure regulation and nitrite homeostasis, with secondary projects that determined differences in vascular tolerance induction by nitroglycerin and nitrite, as well as anesthetic modulated effects on tissue nitrite fluctuations. Subsequent postdoctoral studies at LSU Health Sciences Center-New Orleans queried the importance of nitric oxide (NO) metabolism to neuroendocrine tumor angiogenesis, specifically the role of aldehyde dehydrogenase in tumor angiogenesis and response to anti-angiogenic pharmacological therapies. Dr. Wood is currently a Research Associate in the laboratory of Dr. Adam Straub at the Department of Medicine, University of Pittsburgh.

Dr. Wood’s current research in the Straub lab is focused on determining the role of a novel reduction-oxidation (redox) regulation mechanism -- the CyB5R3-dependent reduction of sGC -- in the control of NO sensitivity in vascular smooth muscle cells (VSMCs) and its impact on SCD vasculopathy. SCD vasculopathy is multifactorial and the pathogenesis remains incompletely understood, although both clinical and experimental evidence concludes that reduced NO bioavailability and/or responsiveness are contributing factors. Dr. Wood researches the impact of this signaling pathway on the development of cardiopulmonary vasculopathy in the humanized transgenic sickle cell mouse (Townes) and chimeras transplanted into tamoxifen-inducible Cre-Lox smooth muscle specific CyB5R3 knock-out and loss of function CyB5R3 T117S polymorphic variants. The overall goal of the research is to test personalized and precision medicine approaches to improve the health of individuals with SCD-associated pulmonary hypertension. Considering the defining role of sGC in NO signaling and the fact that the oxidation state of sGC may predict responses to new classes of sGC activator and stimulator medications, is research aims to significantly impact our understanding of biology, precision therapeutics (right drug for the right patient) and pharmacogenetics (polymorphism based drug selection).

Mingli Liu, MD, PhD

  Teague Cole

Dr. Mingli Liu received her M.D. from Peking University School of Medicine, China. She later completed her postgraduate work in Hematology/Oncology at the People’s Liberation Army Postgraduate Medical School in Beijing, later going on to earn a Ph.D. at Tokyo University, Tokyo, Japan, in the very same field. She is currently an instructor at the Morehouse School of Medicine, in Atlanta, Georgia.

Dr. Liu’s research focuses on identifying signaling pathways associated with pathogenesis of fatal malaria with the goal of targeting upstream molecules in the development of novel interventions. Malaria kills over 500,000 children a year in sub-Saharan Africa and is considered a major global health disparity among economically well off and poorer countries. She and her colleagues have determined that STAT3, a key signaling molecule in the immunity and apoptosis signaling pathways play an important role in the pathogenesis of fatal cerebral malaria (CM) and may be induced by free heme. They have also shown that at physiologically relevant concentrations, heme induces overproduction of CXCL10, a pro-inflammatory, angiostatic, and apoptotic chemokine, in in vitro cultures of human brain microvascular endothelial cells (HBVEC). Overproduction of CXCL10 has been shown to be highly predictive of cerebral malaria mortality in children. This suggests that in addition to parasite-derived cytotoxic agents and host derived inflammatory responses to malaria, the level of free heme in circulation during severe malaria pathogenesis is very critical to the extent of vascular endothelial damage and should be evaluated and controlled during severe malaria prevention, treatment or management. Understanding of the pathogenesis of malaria and a much broader aspect of hemolytic diseases caused by compromised vascular system will help to develop innovative techniques carry out basic and translational hematology research and much-needed new therapiesfor malaria or other hemolytic diseases.