Rate My Professor Dave Kurjiaka

David Kurjiaka is a Professor in the Department of Biomedical Sciences at Grand Valley State University. He received his Ph.D. from Pennsylvania State University, M.S. from the University of Oklahoma, and completed postdoctoral fellowships at the University of Arizona and the John B. Pierce Laboratory at Yale University. His research investigates the impact of inflammatory responses on blood vessel function, directing undergraduate and graduate students in evaluating responses of cultured endothelial and smooth muscle cells to compounds that stimulate or inhibit inflammation. Recent studies focus on the effects of angiotensin II, which decreases capillary and arteriole density in tissues such as the brain and skeletal muscle in hypertension through changes in endothelial cell proliferation or apoptosis, and angiotensin 1-7, which exerts opposite effects via the mas receptor. Kurjiaka's broad training in exercise and comparative physiology supports diverse research questions, including those pursued by honors college students.

Kurjiaka explores the role of gap junctions in vascular function, including cell-to-cell communication that coordinates vessel diameter, vascular resistance, growth, and differentiation of smooth muscle and endothelial cells. His investigations include gap junction-mediated differentiation of mesenchymal cells into smooth muscle cells via connexin 43 and soluble factors from endothelial calcium release, regulation of connexin 40 communication, and diminished vasomotor responses in hypertensive models. He teaches BMS 202 Anatomy Physiology Laboratory, BMS 290 Human Physiology, BMS 495 Concepts in Wellness focusing on cardiovascular disease, and BMS 508 Advanced Human Physiology. Key publications include 'Leukocyte inspired biodegradable particles that selectively and avidly adhere to inflamed endothelium in vitro and in vivo' (Proceedings of the National Academy of Sciences USA, 2003), 'Connexin45 regulates endothelial-induced mesenchymal cell differentiation toward a mural cell phenotype' (Arteriosclerosis, Thrombosis, and Vascular Biology, 2013), 'Chronic hindlimb ischemia impairs functional and vascular reactivity in mouse feed arteries' (Frontiers in Physiology, 2011), 'Hypertension attenuates cell-to-cell communication in hamster retractor muscle feed arteries' (American Journal of Physiology, 2005), and 'Regulation of gap junctional charge selectivity in cells coexpressing connexin 40 and connexin 43' (American Journal of Physiology, 2009).