Jane McHowat
B.Sc., De Montfort University (Pharmacy) and Ph.D. University of Bath (Pharmacology)
Department: Pathology
Academic Rank: Professor
Phone: 314-977-9295 Fax: 314-977-8499
E-mail: mchowaj@slu.edu
Lab Web Page Links: http://path.slu.edu/index.php?page=jane-mchowat-ph-d
Primary Area of Cardiovascular Research Interest
-Endothelial cell-inflammatory cell interactions
-Atherosclerosis
Related Areas of Cardiovascular Research Interest
-Mast cell biology
-T. cruzi-induced myocarditis
-Protease-activated receptors
Summary of Cardiovascular Research Interest
Our current focus in the laboratory is to investigate the biochemical processes that underlie the recruitment of circulating cells to the endothelium during acute and chronic inflammation. More specifically, we are studying the interaction of endothelial cell-derived platelet-activating factor with its corresponding receptor on several cell types. This biochemical and cell function process is currently being applied to several disease states, including atherosclerosis, interstitial cystitis, inflammatory lung diseases and cancer metastases.
Our current studies include the use of endothelial cells isolated from different vascular beds to examine the production of platelet activating factor following activation of calcium independent phospholipase A 2 in response to mast cell mediators, such as tryptase, histamine and TNFa . In addition to biochemical studies, we examine the effect of mast cell mediators on the barrier properties of endothelial and epithelial cells and determine whether these agents affect permeability and/or the rate of wound healing of endothelial and epithelial monolayers.
We are currently using undifferentiated cells isolated from umbilical cord blood as a model for mast cell precursors that are recruited from the circulation to the endothelium. This has lead us to expand our research into the recruitment and homing of undifferentiated cells and to examine the disappearance and appearance of cell surface markers as the cells mature in order to characterize their migratory potential.
In more recent studies, we are using calcium independent phospholipase A 2 mouse models to support our in vitro studies. In these models, we are currently studying the role of endothelial cell calcium independent phospholipase A 2 and platelet-activating factor in lung metastasis development and T. cruzi -induced myocarditis.
