Research Interest: One of my primary interests is to determine whether hereditary hemorrhagic telangiectasia (HHT) confers a pro-coagulant state in HHT patients. Another very interesting aspect of HHT we are attempting to resolve is the role of iron deficiency anemia in potentiating thrombosis risk in HHT, particularly the molecular mechanism that elevates the plasma levels of both Factor VIII and von Willebrand factor (vWF) in HHT patients.
Secondly, our lab is also trying to decipher the very important yet unanswered aspects of the classical Myeloproliferative Neoplasm (MPN) which associates to thrombotic events even after it’s diagnosis (~25%). The variant allele fraction (VAF) of JAK2V617F, the most common MPN driver mutation (~70% of all cases), has been positively correlated to neutrophil expression of hypoxia-inducible factor alpha (HIFα)-mediated genes including plasminogen activator inhibitor 1 (PAI-1) and tissue factor (TF) along with subsequent thrombosis history. The most interesting part is that some preliminary data from our lab challenge the long-standing dogma that neutrophils only passively acquire TF. Thus, our goal is to try to determine the effects of JAK2V617F gene dosage and the role of HIFα in MPN associated venous thrombosis (VT) using a murine model of IVC stenosis.
