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Research summary

My program of research focuses on the regulation of mitochondrial function and metabolism during cardiac and skeletal muscle differentiation and remodeling, including disease related conditions such as hypoxia/ischemia, diabetic cardiomyopathy, and insulin resistance; as well as physiological stimuli such as exercise and contractile activity. My laboratory utilizes cellular, molecular, and multi-omics approaches to understand mitochondrial function, dynamics, and turn-over including the regulation of mitophagy and mitochondrial permeability transition. Specifically, my laboratory studies the transcriptional regulation and post-translational modification of the Bcl-2 family members Nix and Bnip3 utilizing both primary and immortalized cells, differentiated human induced pluripotent stem cells, and conditional knockout mice.

Biography

Over the course of my training, I have studied in 3 high-profile Canada research laboratories, each with a track-record for excellence. I began my graduate training with Dr. David Hood in the School of Kinesiology and Health Science at York University. During my MSc training with Dr. Hood, I studied how skeletal muscle mitochondria physiologically adapt to chronic contractile activity, with a specific interest in the mitochondrial protein import pathway and the molecular regulation of the mitochondrial transcription factor A (Tfam). During my PhD training, I studied with Dr. John McDermott in the Department of Biology at York University. Here, I examined the importance of the myocyte enhancer factor 2 (MEF2) family of transcription factors in muscle differentiation. My dissertation was directed toward understanding how protein kinase A (PKA) negatively regulates MEF2 activity and muscle gene transcription. In addition, we identified a novel MEF2 interacting partner, the protein phosphatase 1α, and determined how this mechanism regulates myocardin expression in vascular smooth muscle cells through CPI-17. Finally, I trained as a postdoctoral fellow with Dr. Lorrie Kirshenbaum at the St. Boniface Research Centre, where I studied the molecular regulation of hypoxia-induced programmed cell death in cardiac myocytes. Here, I was involved in the discovery and biological characterization of a novel hypoxia-inducible splice variant of the death-gene Bnip3. We discovered that this splice variant acts as an endogenous inhibitor, serving to promote cardiac myocyte survival.

As an independent scientist, I am pursuing my own experimental interests, such as muscle lipotoxicity and diabetes-associated complications of the cardiovascular system. Although my program is based on the expertise I acquired during my training, all current projects in my laboratory are based on novel observations since I became independent. Current projects in my laboratory involve: 1) the regulation of Nix by Myocardin during cardiac development and disease; 2) the evaluation of Nix-induced mitophagy and the role in muscle and heart insulin resistance; 3) determining how Bnip3 regulates neonatal cardiomyocyte cell death and proliferation during hypoxic injury; and 4) evaluating the role of Nix and Bnip3 in rhabdomyosarcoma.

Education

Awards

  • CIHR-MHRC Post-doctoral fellowship (2011–2012)
  • CIHR IMPACT Strategic Training Program Post-doctoral fellowship (2011-2012)
  • Arnold Naimark Young Investigator Award (2011)

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