Patrick A. Murphy, PhD

Disturbed blood flow patterns can lead to chronic inflammatory conditions in the arterial wall, a precipitating event in cardiovascular components of heart attack and stroke. The Murphy lab is dissecting the interactions between recruited immune cells and the arterial wall using inducible genetic models combined with intravital imaging, and in vitro co-culture models under varying flow regimes. We are endothelial-centric and focused on changes in alternative splicing and the sub-endothelial extracellular matrix induced by innate immune cell recruitment, which our data suggests play an important role in the progression of arterial inflammation. A deeper understanding of how the endothelium interacts with recruited immune cells will reveal ways to intervene with the processes underlying the growth and rupture of aneurysms and atherosclerotic plaques.

[2026] Transcriptomic profiles from normal and tumor tissue samples reveal distinct venule populations and novel tumor endothelial cell markers in breast cancer. [2025] Amyotrophic lateral sclerosis and frontotemporal dementia mutation reduces endothelial TDP-43 and causes blood-brain barrier defects. [2025] Endothelial TDP-43 depletion disrupts core blood-brain barrier pathways in neurodegeneration. [2024] Contribution of amyloid deposition from oligodendrocytes in a mouse model of Alzheimer's disease. [2024] Autoregulated splicing of TRA2β programs T cell fate in response to antigen-receptor stimulation. [2024] Endothelial Immunosuppression in Atherosclerosis : Translational Control by Elavl1/HuR. [2023] Loss of Endothelial TDP-43 Leads to Blood Brain Barrier Defects in Mouse Models of A