Damon Poburko at a glance

Education:

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

Contact:

email: dpoburko@sfu.ca, phone: 778.782.9464

Publications:

Pubmed Articles

Google Scholar

Social Media:

Research Interests

My lab focuses on the mechanisms that regulate Ca2+ signaling, contraction and phenotype in vascular smooth muscle. Our interests fall into two themes:

MOLECULAR & CEllULAR PHYSIOLOGY OF THE SYMPATHETIC NEUROVASCULAR INTERFACE

Sympathetic nerves regulator vascular tone by releasing norepinephrine and co-transmitters like ATP, neuropeptide Y, and beta-nicotinamide adenine dinucleotide. My lab studies the mechanisms that regulate "co-release", and how such “co-release” can be altered physiologically and in vascular pathologies like hypertension. We use fluorescence microscopy, wire myography, and molecular techniques to study how ATP and norepinephrine are differentially stored and released from sympathetic nerves and cultured cells. We also develop molecular probes to optically monitor the release of ATP. 

MITOCHONDRIA IN VASCULAR PHYSIOLOGY AND AGING

High blood pressure is a major risk factor for cardiovascular disease, which is the leading cause of death in the developed world. High blood pressure commonly stem from narrowing of blood vessels due to excess vasoconstriction and the thickening of vascular walls. Mitochondrial dysfunction promotes vascular remodeling and affects vascular smooth muscle contractility and phenotype. Mitochondria are also a common target of chronic inflammation, stress, diabetes and obesity. We use cell and organ cultures to study how diverse insults experienced by blood vessels impact mitochondrial health, and how this impacts smooth muscle phenotype and cell cycle. We use high content imaging assays, wire myography, and molecular analyses of gene  expression and mitochondrial DNA modification to understand the interplay between mitochondrial dysfunction and its impact on smooth muscle physiology.