Contact info

Dr Michael A. Rudnicki
Sprott Centre for Stem Cell Research
Ottawa Hospital Research Institute
501, Smyth Road - Room 5105
Ottawa, ON K1H 8L6

Tel: 1-613-739-6740
Fax: 1-613-739-6294
E-mail: [email protected]

Link to Rudnicki Lab webpage

Research keywords

Dr Michael Rudnicki is a Senior Scientist and the Director of the Regenerative Medicine Program and the Sprott Centre for Stem Cell Research at the Ottawa Hospital Research Institute. He is Professor in the Department of Medicine at the University of Ottawa. Dr Rudnicki is the Scientific Director of the Canadian Stem Cell Network.

Dr Rudnicki received his PhD at the University of Ottawa in 1988 with Dr Michael McBurney where he examined the cardiac-specific control of gene expression during embryonal carcinoma cell differentiation. Dr Rudnicki trained at the post-doctoral level at the Massachusetts Institute of Technology in the Whitehead Institute with Dr Rudolf Jaenisch. His post-doctoral studies involved the genetic dissection of the function of the MyoD-family of transcription factors by gene targeting. Dr Rudnicki was appointed Assistant Professor at McMaster University in 1992. He moved to Ottawa In 2000 to join the Ottawa Health Research Institute.

Dr Rudnicki is a Fellow of the Royal Society of Canada, he holds the Canada Research Chair in Molecular Genetics, and is an International Research Scholar of the Howard Hughes Medical Institute. He is an Associate Editor of the Journal of Cell Biology and Cell Stem Cell, and has organized international research conferences as one of the founding directors of the Society for Muscle Biology. He holds operating grants from the National Institutes of Health, the Canadian Institutes of Health Research, the Muscular Dystrophy Association, and the Howard Hughes Medical Institute.

Click here for pdf CV

Dr Rudnicki's laboratory works to understand the molecular mechanisms that regulate the determination, proliferation, and differentiation of stem cells during embryonic development and during tissue regeneration. The lab has conducted extensive studies into both embryonic myogenesis and the function of stem cells in adult regenerative myogenesis. Towards this end, the lab employs molecular genetic and genomic approaches to determine the function and roles played by regulatory factors. They identified Pax7 as a transcription factor required for the specification of satellite cells, and identified Wnt signaling as playing an important role in muscle stem cell function. His research has been published in scientific journals that include Cell, Nature Cell Biology, Cell Stem Cell, Genes & Development, and PLoS Biology.

Click here for PubMed listing

There are no known therapeutic drugs for pancreatic tissue repair, in particular, for the growth or regeneration of the islet β-cells that produce insulin. However, it is known that the pancreas is capable of self-regeneration following a removal of a portion of the pancreas. Consequently, we set out to identify genes induced during pancreatic regeneration following partial removal of the pancreas in mice. We performed a gene expression screen comparing undamaged pancreas and the regenerating pancreas at three days following surgery. We identified a secreted protein that has also been shown to increase cell mobility. Notably, mice without the gene were unable to regenerate their pancreas whereas injection of the protein stimulated a marked increase in the number of insulin expressing islets and induced formation of new islets and enhanced insulin production in diabetic mice.

To extend these studies, we are examining the pancreatic phenotype of mice lacking the gene. We are performing experiments to determine whether mice lacking the gene are more prone to develop diabetes in response to chemical agents that damage the pancreas, or as they age. We will investigate approaches to utilize the protein to reverse diabetes in experimental animals. Pancreas regeneration induced by injection of the protein will be evaluated at the tissue level and by monitoring of blood glucose levels, and glucose tolerance testing. We are also performing experiments to compare different isoforms and to see if shorter portions of the protein can be used. Together, these experiments will provide important new insights into the mechanisms that regulate regeneration in the pancreas and determine whether the candidate protein has the potential to be used therapeutically for the treatment of Type 1 Diabetes. The project is funded through the JDRF Academic R&D; Program.