Researcher

    Nicolas Dumont , Pht , Ph.D.

    nicolas.dumont@recherche-ste-justine.qc.ca
    Nicolas Dumont
    Research Axis
    Musculoskeletal Diseases and Rehabilitation
    Address
    CHUSJ - Centre de Recherche

    Phone
    514 345-4931 #3263

    Title

    • Associate professor, Rehabilitation Department, Faculty of Medicine, Université de Montréal (2016)

    Education

    • Postdoctoral fellow in regenerative medicine, Ottawa Hospital Research Institute, University of Ottawa Ottawa, ON, Canada (2013-2016)
    • PhD in physiology-endocrinology, CHUQ Research Center, Université Laval, Quebec city, QC, Canada (2007-2013)
    • MSc in physiology-endocrinology, CHUQ Research Center, Université Laval, Quebec city, QC, Canada (2005-2007)
    • BSc in physiotherapy, Université Laval, Quebec city, QC, Canada (2002-2005)

    Research Topics

    • Muscle regeneration
    • Duchenne muscular dystrophy
    • Muscle stem cell (satellite cell)
    • Atrophy and growth of skeletal muscles
    • Acute and chronic inflammation
    • Cell polarity and asymmetric cell division
    • Self-renewal, proliferation and differentiation of satellite cells

    Career Summary

    Nicolas Dumont is an associate professor at the Department of Rehabilitation of the University of Montreal and a principal investigator at the CHU Sainte-Justine Research Center. The research interests of its laboratory focus on the understanding of muscular pathologies and their impacts on satellite cells, a population of adult muscle stem cells that is responsible of skeletal muscle regeneration. Its recent work demonstrated that satellite cells have cell-autonomous defects in Duchenne muscular dystrophy, a severe genetic disease leading to progressive and irreversible muscle wasting. The objective of research projects performed the laboratory is to define how extrinsic factors, such as inflammation and fibrosis, affect muscle regeneration in physiological and pathological conditions. Ultimately, these findings could lead to the development of therapies that rescue the cell-autonomous defects of satellite cells in Duchenne muscular dystrophy (or other muscle pathologies) and transform this lethal debilitating disease into a chronic manageable condition. 

    Awards and Distinctions

    • CHIR post-doctoral fellowship (2013-2016) 
    • FRSQ doctoral research award (2009-2012)
    • Laval University Foundation doctoral research award (2008-2009)

    Presentations

    • Dumont NA. Dysfonction des cellules souches musculaires dans la dystrophie musculaire de Duchenne. Scientific conference of the musculoskeletal diseases and rehabilitation axis. Ste-Justine Hospital. Montreal. January 2016. *Note : Invited speaker
    • Dumont NA, Wang XY, von Maltzahn J, Pasut A, Bentzinger CF, Brun CE, Rudnicki MA. Muscle Stem Cell Dysfunction in Duchenne Muscular Dystrophy. Till and McCulloch annual meeting. Toronto. November 2015
    • Dumont NA, Wang XY, von Maltzahn J, Pasut A, Bentzinger CF, Brun CE, Rudnicki MA. Muscle Stem Cell Dysfunction in Duchenne Muscular Dystrophy. 3rd Ottawa international conference on neuromuscular biology. Ottawa. September 2015
    • Dumont NA, Wang YX, Von Maltzhan J, Pasut A, Bentzinger CF, Brun CE & Rudnicki MA. Dystrophin and satellite cell polarity. OHRI research day. Ottawa. July 2015. *Note : Won the first prize for oral presentation
    • Dumont NA, Wang XY, von Maltzahn J, Pasut A, Bentzinger CF, Brun CE, Rudnicki MA. Muscle Stem Cell Dysfunction in Duchenne Muscular Dystrophy. Gordon research conference on Myogenesis. Lucca, Italy. June 2015. *Note : Won the first prize for poster presentation
    • Dumont NA, von Maltzahn J, Bentzinger CF, Rudnicki MA. Dystrophin is required for muscle stem cell asymmetric division. OHRI research day. Ottawa. November 2014
    • Dumont NA, von Maltzahn J, Bentzinger CF, Rudnicki MA. Dystrophin is required for muscle stem cell asymmetric division. Till & McCulloch annual meeting. Ottawa. November 2014.
    • Dumont NA, von Maltzahn J, Bentzinger CF, Rudnicki MA. Dystrophin is required for muscle stem cell asymmetric division. Center for neuromuscular disorders research day. Ottawa. October 2014.
    • Dumont NA, Bentzinger CF, Nhan K, Rudnicki MA. Fzd7 affects myogenic cells in a Wnt7a-dependent and independent manner. FASEB Conference. Steamboat springs, CO, USA. July 2014
    • Dumont NA, Dufresne SS, Bouchard P, Lavergne E, Piette AB, Sarao R, Penninger JM and Frenette J. Inhibition of RANK/RANKL pathway greatly improves SERCA activity and force production in atrophic and dystrophic skeletal muscles. 7th cachexia conference. Kobe, Japan. December 2013.
    • Dumont NA, Bentzinger CF, Rudnicki MA. Fzd7 receptor represses satellite cell proliferation. OHRI research day. Dumont NA, Dufresne SS, Bouchard P, Lavergne E, Piette AB, Sarao R, Penninger JM and Frenette J. Blockade of receptor activator of nuclear factor-κB signaling greatly improves SERCA activity and contractility in atrophic and dystrophic skeletal muscles. FASEB conference. Vermont, USA. July 2013.
    • Dumont N., Dufresne SS., Godbout C., Sarao R., Bouchard P., Lavergne E., De la Durantaye M., Penninger JM, Frenette J. RANK/RANKL/OPG pathway modulates SERCA activity and expression and is a novel and important actor of skeletal muscle pathology and dysfunction. Gordon research conference on Calcium signaling, Lucca, Italy. June 2013
    • Dumont NA, Frenette J. Optimization of macrophage-secreted myogenic factors and promotion of muscle regrowth. Society on sarcopenia, cachexia and wasting disorders – 6th cachexia conference. Milan, Italy. December 2011
    • Dumont NA. Les leucocytes et leurs médiateurs dans la récupération du muscle atrophié. CHUQ Neurosciences axis seminar series. Quebec city. October 2010. *Note: invited speaker
    • Dumont NA, Frenette J. Muscle atrophy and regrowth: is it time to modify our perception of the inflammatory reaction? 12th research colloquium on rehabilitation. Centre for interdisciplinary research in rehabilitation of greater Montreal. Montreal. June 2010
    • Dumont NA, Frenette J. Inflammation et croissance du muscle atrophié: le rôle myogénique des macrophages. 12th annual research day of the Faculty of Medicine of Laval University. Quebec city. May 2010. 
    • Dumont N, Frenette J. Macrophages protect against muscle atrophy and promote muscle recovery in vivo and in vitro: a mechanism partly dependent on the IGF-1 signaling molecule. Society on sarcopenia, cachexia and wasting disorders – 5th cachexia conference. Barcelona, Spain. December 2009
    • Dumont N, Frenette J. Macrophages protect against muscle atrophy and promote muscle recovery in vivo and in vitro: a mechanism partly dependent on the IGF-1 signaling molecule. American Society for Cell Biology – 49th annual meeting. San Diego, CA, USA. December 2009. 
    • Dumont N, Frenette J. Neutrophils invade atrophied skeletal muscles without causing muscle dysfunction unless they are stimulated with LPS. American college of sport medicine – 55th annual meeting. Indianapolis, IN, USA. May 2008.

    Most Important Publications

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Edited by Hoffmann Maude

Created on 9/18/2014
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