Dr. Cowan completed a PhD in cardiovascular research under the supervision of Dr. Marlene Rabinovitch at the Hospital for Sick Children, Department of Laboratory Medicine and Pathobiology, University of Toronto where he studied the pathophysiology of primary arterial hypertension and approaches to its reversal. He then started medical studies at the University of Toronto, which followed by a 5 years of general surgery residency at the University of Western Ontario. During his residency, Dr. Cowan continued his basic science training with the completion of a post-doctoral fellowship in the area of cell communication (connexins and pannexins) and tumor biology in the laboratory of Dr. Dale W. Laird at the University of Western Ontario, Department of Anatomy and Cell Biology. After finishing his general surgery residency and postdoctoral fellowship in 2009, Dr. Cowan completed a paediatric surgery fellowship (2009-2011) at CHEO.
Dr. Cowan is the recipient of numerous awards, including the Canadian Institute of Health Research and the Canadian Society for Clinical Investigation joint Resident Research Award, Physician Services Incorporated Foundation Resident Research Award, and the American College of Cardiology Young Investigator’s Award.
Identification of pannexin 1-regulated genes, interactome, and pathways in rhabdomyosarcoma and its tumor inhibitory interaction with AHNAK.
Using this unbiased genome-wide approach, our transcriptomic analysis identified the genes that are regulated in PANX1-expressing RMS cells together with the key cellular processes in which they may be involved.
Pannexin 1 inhibits rhabdomyosarcoma progression through a mechanism independent of its canonical channel function
The comparison of PANX1 direct interactors in RMS cells to that of skeletal muscle myoblasts may also enable a better understanding of the mechanisms activating and inhibiting PANX1 channels in physiologic and pathologic processes.
Expression of Pannexin 1 and Pannexin 3 during skeletal muscle development, regeneration, and Duchenne muscular dystrophy.
These findings suggest that Panx1 and Panx3 channels may play important and distinct roles in healthy and diseased skeletal muscles.
Pannexin 1 and Pannexin 3 Channels Regulate Skeletal Muscle Myoblast Proliferation and Differentiation
Collectively, our results reveal that both Panx1 and Panx3 are expressed in skeletal muscle myoblasts and that their levels are differentially modulated during the differentiation process regulating either myoblast proliferation and/or differentiation status.