A5039776242- Muscle Physiology and Disorders
- Tissue Engineering and Regenerative Medicine
- Genetics, Aging, and Longevity in Model Organisms
- Adipose Tissue and Metabolism
- Neurogenetic and Muscular Disorders Research
- Mesenchymal stem cell research
- Genetic Neurodegenerative Diseases
- Genetics and Neurodevelopmental Disorders
- Pluripotent Stem Cells Research
- Telomeres, Telomerase, and Senescence
- Digestive system and related health
- Muscle metabolism and nutrition
- Birth, Development, and Health
- Wnt/β-catenin signaling in development and cancer
- Connective tissue disorders research
- Cell Adhesion Molecules Research
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- PI3K/AKT/mTOR signaling in cancer
- Spaceflight effects on biology
- Genetics and Physical Performance
- Apelin-related biomedical research
- Autophagy in Disease and Therapy
- Connective Tissue Growth Factor Research
- Cardiac Fibrosis and Remodeling
- Peroxisome Proliferator-Activated Receptors
Centre Hospitalier Universitaire de Sherbrooke
2020-2025
Université de Sherbrooke
2017-2024
Nestlé (Brazil)
2022
Nestlé (Switzerland)
2015-2022
École Polytechnique Fédérale de Lausanne
2015-2020
Ottawa Hospital Research Institute
2011-2015
Ottawa Hospital
2011-2015
University of Ottawa
2013-2015
University of Basel
2005-2014
Stem Cell Network
2010-2012
Wnt7a/Fzd7 signaling stimulates skeletal muscle growth and repair by inducing the symmetric expansion of satellite stem cells through planar cell polarity pathway activating Akt/mTOR in fibers. Here we describe a third level activity where increases directional migration mouse human myogenic progenitors activation Dvl2 small GTPase Rac1. Importantly, these effects can be exploited to potentiate outcome transplantation into dystrophic muscles. We observed that short Wnt7a treatment markedly...
Abstract Background Skeletal muscle mass is determined by the balance between protein synthesis and degradation. Mammalian target of rapamycin complex 1 (mTORC1) a master regulator translation has been implicated in control mass. Inactivation mTORC1 skeletal muscle-specific deletion its obligatory component raptor results smaller muscles lethal dystrophy. Moreover, raptor-deficient are less oxidative through changes expression PGC-1α, critical determinant mitochondrial biogenesis. These...
Mutations in the gene encoding alpha2 subunit of laminins cause severe "merosin-deficient congenital muscular dystrophy" (MDC1A). We have recently shown that overexpression a miniaturized form molecule agrin (mini-agrin) counteracts disease dy(W)/dy(W) mice, model for MDC1A. However, these mice express some residual truncated laminin-alpha2, suggesting observed amelioration might be due to mini-agrin's presenting laminin-alpha2 its receptors. Here we show mini-agrin dy(3K)/dy(3K) which are...
Wnt signaling has essential roles during embryonic development and tissue homoeostasis. proteins are post-translationally modified the attachment of a palmitate moiety at two conserved residues is believed to be prerequisite for secretion function proteins. Here we demonstrate that mammalian protein can fully functional without palmitoylation. We generate truncated Wnt7a variant, consisting C-terminal 137 amino acids lacking palmitoylation sites show it retains full biological activity in...
Wnt-mediated signals are involved in many important steps mammalian regeneration. In multiple cell types, the R-spondin (Rspo) family of secreted proteins potently activates canonical Wnt/β-catenin pathway. Here, we identify Rspo1 as a mediator skeletal muscle tissue repair. First, show that deletion results global alteration regeneration kinetics following acute injury. We find progenitor cells lacking delayed differentiation due to reduced activation target genes. Furthermore, have fusion...
Impaired skeletal muscle stem cell (MuSC) function has long been suspected to contribute the pathogenesis of muscular dystrophy (MD). Here, we showed that defects in endothelial (EC) compartment vascular niche mouse models Duchenne MD, laminin α2–related and collagen VI–related myopathy were associated with inefficient mobilization MuSCs after tissue damage. Using chemoinformatic analysis, identified 13–amino acid form peptide hormone apelin (AP-13) as a candidate for systemic stimulation...
Mammalian target of rapamycin complex 1 (mTORC1) is central to the control cell, organ, and body size. Skeletal muscle-specific inactivation mTORC1 in mice results smaller muscle fibers, fewer mitochondria, increased glycogen stores, a progressive myopathy that causes premature death. In mTORC1-deficient muscles, peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α), which regulates mitochondrial biogenesis glucose homeostasis, strongly down-regulated. Here we tested...
Increasing evidence suggests that the muscle stem cell (MuSC) pool is heterogeneous. In particular, a rare subset of PAX7-positive MuSCs has never expressed myogenic regulatory factor MYF5 displays unique self-renewal and engraftment characteristics. However, scarcity limited availability protein markers make characterization these cells challenging. Here, we describe generation StemRep reporter mice enabling monitoring PAX7 proteins based on equimolar levels dual nuclear fluorescence. High...