About Damon Poburko
B.Sc. (Co-op) Pharmacology & Therapeutics, University of British Columbia – 2001
Ph.D., Pharmacology & Therapeutics, University of British Columbia – 2005
Postdoctoral: University of Geneva – 2006-2008
Postdoctoral: Stanford University – 2008-2011
email: email@example.com, phone: 778.782.9464
My lab's research centres on understanding the molecular underpinning of vascular health and function. This generally falls into two areas of interest: How nerves co-release multiple neurotransmitters like ATP and norepinephrine and how mitochondria help maintain smooth muscle cells in a quiescent and contractile state or phenotype.
ATP Secretion and neurotransmitter co-release
The stimulation of blood vessels by sympathetic nerves is a primary regulator of vascular tone. While these nerves are best known for stimulating contraction by releasing norepinephrine, they also release co-transmitters like ATP, neuropeptide Y, and beta-nicotinamide adenine dinucleotide. I am interested in the mechanisms that regulate which of these neurotransmitters are released, and how such “co-release” can be altered physiologically, as well as how they contribute to vascular pathologies like hypertension. We employ fluorescence microscopy, wire myography, and other molecular techniques to examine how ATP and norepinephrine are differentially stored and released from sympathetic nerve endings in rat blood vessels. We are also developing novel molecular probes to directly, and for the first time, monitor the release of ATP from individual synaptic varicosities, and are developing novel assays to image the release of synaptic vesicles in intact blood vessels.
mitochondrial DNA and smooth muscle physiology
High blood pressure is a major risk factor for cardiovascular disease, the leading cause of death in the developed world. Two common causes of high blood pressure are the narrowing of blood vessels due to excess vasoconstriction and the thickening of vascular walls due to smooth muscle proliferation (i.e. remodelling). There is growing recognition that both acute and chronic formation of mitochondrial dysfunction promotes vascular remodeling, and affects vascular smooth muscle contractility and phenotype. In this regard, mitochondria are a common target of chronic inflammation, stress, diabetes and obesity. My lab is using cell and organ cultures to examine how noxious stimuli commonly experienced by blood vessels impact mitochondrial health, and how this affects smooth muscle phenotype and cell cycle. We employ high content imaging assays, wire myography, molecular analyses of gene transcription, and mitochondrial DNA modification to better understand the interplay between mitochondrial dysfunction and its impact on smooth muscle physiology.
Within the department of Biomedical Physiology and Kinesiology, I teach a range of undergraduate courses.
An introduction to contemporyary health
An introductory survey of human physiology with an emphasis on mechanisms of regulation and integration. This course discusses anatomical structures relevant to the functional of major organ systems, and covers the basic functioning of all major organ systems of the human body. While this is intended as a survey course, some topics will be covered in reasonable detail in order to give insight into mechanisms of function.
An advanced course in cardiovascular and respiratory physiology. We cover topics with an integrative perspective; from molecule to system level physiology. Discussion of the mechanisms of a range of cardiovascular and respiratory diseases is used to describe and understand physiology in health and disease.
A specialized course in cellular and moleculare vascular physiology. This course covers vascular development, advanced topics in contractile regulation and aspects of angiongenesis and remodelling. Student engage in primary literature in instructor-led tutorials and conduct a miniture literature-based research project.