Our mission is to significantly contribute to a better understanding of the causes and consequences of small blood vessel pathologies in disease. We strive to create a productive and positive research environment in which we can utilize a team-based approach to discover cellular and molecular mechanisms involved in microvascular pathobiology. We are committed to training the future generations of scientists and science-based clinicians. Our lab employs a multifaceted experimental approach ranging from state-of-the-art molecular and cell biology techniques, in vitro, to extensive pathophysiological analyses of relevant disease models, in vivo.
Intercellular, cellular-matrix, and matrix-cellular signaling as it relates to microvascular barrier (dys)function.
Our lab focuses on microvascular pathobiology and the elucidation of mechanisms for endothelial barrier dysfunction during aberrant inflammatory responses. Though all endothelial cells throughout the vascular system have some barrier properties, the blood-brain barrier (BBB) endothelia in the brain microcirculation are the most finely-tuned and structurally competent. BBB dysfunction is a key pathologic component of several CNS diseases associated with aberrant inflammation such as multiple sclerosis, Parkinson’s, traumatic brain injury, stroke, Binswanger’s, and Alzheimer’s disease. We are particularly interested in the signal transduction that controls endothelial cell-cell adhesion in both homeostasis and inflammation. What impels us the most to continue studying this topic is it’s potential to have a major impact on a multitude of disorders that contribute to a substantial economic burden on our society.
Our lab focuses on two overarching projects:
1) Cytokine-induced transcriptional repression of microvascular endothelial tight junctions during inflammatory responses.
2) The influence of matrix-endothelial interactions on endothelial cell-cell adhesion.