About Aaron Mickle
Aaron Mickle is an Assistant Professor in the Department of Physiological Sciences, in the College of Veterinary Medicine at the University of Florida. His current research focuses on incorporating multiple techniques at the system and cellular level to answer questions related to mechanisms of bladder sensory function and pain.
Development of technology to study visceral diseases and refine current/develop new analgesic technologies – Our lab works closely with material, chemical and electrical engineers to develop new tools to study the nervous system with the end goal using these tools to study the changes that occur in these systems during and after the development of chronic pain, as well as the hopeful end goal of implementing these strategies in patients.
Urothelial cell-to-sensory afferent signaling in bladder pain and function – Urothelial cells, the endothelial cells that line the bladder wall, were classically thought to function as a passive barrier. However, evidence collected over the last decade has shown them to be a much more active component of bladder physiology and pathophysiology. The fact that urothelial cells express many different types of sensory receptors, ion channels, signaling peptides and neurotransmitters, along with their close proximity to nerve fibers suggest that they could communicate and/or receive input from neuronal cells. Our lab is using innovative techniques to isolate these signaling mechanisms to specific cell types with the goal of understanding how these cells communicate under normal physiologic conditions as well as how the signaling may be altered under disease conditions.
The role of immune cell signaling in interstitial cystitis/ bladder pain syndrome (IC/BPS) pain – IC/BPS is idiopathic in nature, however over the past two decades mounting evidence suggests alterations to the innate immune response may play a role in the symptomology and progression of the disease. Our lab aims to study the involvement of different immune cells in pain and bladder dysfunction associated with models of IC/BPS
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