We are working on the signal transduction pathways triggered by the growth factor FGF-2 in cardiac myocytes leading to (a) proliferation, (b) protection from injury and cell death and (c) affecting cardiac gap junction channels. In (a) we are focusing on eliminating signals that are antagonistic to the proliferative effect of FGF-2. In (b) we are examining FGF-2 and its mutants as potential therapeutic agents in the context of 'reperfusion injury' that occurs during a heart attack. In (c) we use structure function studies of the gap junction protein connexin-43, to identify regions involved in the regulation of cardiac cell to cell communication (related to arrhythmias) and growth.
Academic AchievementsResearch Interests
We are examining the role of growth factors and their receptors in the heart in the context of:
- Myocardial Injury: (I) Regeneration. Use of cell and molecular biology techniques (macromolecule biochemistry, immunocytochemistry, in situ hybridization, gene transfer, micromanipulation) to understand mechanisms controlling the regenerative ability of cardiac myocytes in adult hearts. We employ primary cultures of cardiac cells and in vivo models of myocardial infarction.
- Myocardial Injury: (II) Protection. Use of cell physiology and molecular biology techniques to examine the cardioprotective role of endogenous or administered factors. We employ an isolated rat heart perfusion model.
- Intercellular Communication. We study regulation of expression and function of cardiac gap junction proteins, in development and after injury, in a rat model, using cell/molecular biology and cell physiology techniques.
St. Boniface Research Ctr
Inst Cardiovascular Sciences
R3008 - 351 Tache Ave
Winnipeg MB CANADA
R2H 2A6
Tel: 204 235 3519
204 79 3823
Fax 204 233 6723