Search

Your search keyword '"Dumont, Nicolas A."' showing total 24 results
Start Over Author "Dumont, Nicolas A." Publication Year Range Last 3 years
24 results on '"Dumont, Nicolas A."'

3. Clearance of defective muscle stem cells by senolytics restores myogenesis in myotonic dystrophy type 1

Author

Conte, Talita C., Duran-Bishop, Gilberto, Orfi, Zakaria, Mokhtari, Inès, Deprez, Alyson, Côté, Isabelle, Molina, Thomas, Kim, Tae-Yeon, Tellier, Lydia, Roussel, Marie-Pier, Maggiorani, Damien, Benabdallah, Basma, Leclerc, Severine, Feulner, Lara, Pellerito, Ornella, Mathieu, Jean, Andelfinger, Gregor, Gagnon, Cynthia, Beauséjour, Christian, McGraw, Serge, Duchesne, Elise, and Dumont, Nicolas A.

Published
2023
Full Text
View/download PDF

7. N -acetylneuraminate pyruvate lyase controls sialylation of muscle glycoproteins essential for muscle regeneration and function

Author

Da Silva, Afitz, primary, Dort, Junio, additional, Orfi, Zakaria, additional, Pan, Xuefang, additional, Huang, Sjanie, additional, Kho, Ikhui, additional, Heckel, Emilie, additional, Muscarnera, Giacomo, additional, van Vliet, Patrick Piet, additional, Sturiale, Luisa, additional, Messina, Angela, additional, Romeo, Donata Agata, additional, van Karnebeek, Clara D.M., additional, Wen, Xiao-Yan, additional, Hinek, Aleksander, additional, Molina, Thomas, additional, Andelfinger, Gregor, additional, Ellezam, Benjamin, additional, Yamanaka, Yojiro, additional, Olivos, Hernando J., additional, Morales, Carlos R., additional, Joyal, Jean-Sébastien, additional, Lefeber, Dirk J., additional, Garozzo, Domenico, additional, Dumont, Nicolas A., additional, and Pshezhetsky, Alexey V., additional

Published
2023
Full Text
View/download PDF

13. Apelin Stimulation of the Perivascular MuSC Niche Enhances Endogenous Repair in Muscular Dystrophy

Author

Le Moal, Emmeran, primary, Liu, Yuguo, additional, Collerette-Tremblay, Jasmin, additional, Dumontier, Simon, additional, Boutin, Joël, additional, Dort, Junio, additional, Orfi, Zakaria, additional, Michaud, Joris, additional, Giguère, Hugo, additional, Desroches, Alexandre, additional, Trân, Kien, additional, Vézina, François, additional, Bedard, Sonia, additional, Raynaud, Catherine, additional, Balg, Frederic, additional, Sarret, Philippe, additional, Scott, Michelle S., additional, Feige, Jerome N., additional, Denault, Jean-Bernard, additional, Dumont, Nicolas A., additional, Marsault, Eric, additional, Auger-Messier, Mannix, additional, and Bentzinger, C. Florian, additional

Published
2022
Full Text
View/download PDF

14. Clearance of defective muscle stem cells by senolytics reduces the expression of senescence-associated secretory phenotype and restores myogenesis in myotonic dystrophy type 1.

Author

Conte, Talita, primary, Bishop, Gilberto Duran, additional, Orfi, Zakaria, additional, Mokhtari, Ines, additional, Deprez, Alyson, additional, Roussel, Marie-Pier, additional, Cote, Isabelle, additional, Pellerito, Ornella, additional, Maggiorani, Damien, additional, Benabdallah, Basma, additional, Leclerc, Severine, additional, Feulner, Lara, additional, Mathieu, Jean, additional, Gagnon, Cynthia, additional, Andelfinger, Gregor, additional, Beausejour, Christian, additional, McGraw, Serge, additional, Duchesne, Elise, additional, and Dumont, Nicolas, additional

Published
2022
Full Text
View/download PDF

15. An engineered multicellular stem cell niche for the 3D derivation of human myogenic progenitors from iPSCs

Author

Mashinchian, Omid, primary, De Franceschi, Filippo, additional, Nassiri, Sina, additional, Michaud, Joris, additional, Migliavacca, Eugenia, additional, Aouad, Patrick, additional, Metairon, Sylviane, additional, Pruvost, Solenn, additional, Karaz, Sonia, additional, Fabre, Paul, additional, Molina, Thomas, additional, Stuelsatz, Pascal, additional, Hegde, Nagabhooshan, additional, Le Moal, Emmeran, additional, Dammone, Gabriele, additional, Dumont, Nicolas A, additional, Lutolf, Matthias P, additional, Feige, Jerome N, additional, and Bentzinger, C Florian, additional

Published
2022
Full Text
View/download PDF

16. Cover Image, Volume 237, Number 4, April 2022

Author

Soulez, Mathilde, primary, Tanguay, Pierre‐Luc, additional, Dô, Florence, additional, Dort, Junio, additional, Crist, Colin, additional, Kotlyarov, Alexey, additional, Gaestel, Matthias, additional, Ferron, Mathieu, additional, Dumont, Nicolas A., additional, and Meloche, Sylvain, additional

Published
2022
Full Text
View/download PDF

22. Apelin stimulation of the vascular skeletal muscle stem cell niche enhances endogenous repair in dystrophic mice

Author

Le Moal, Emmeran, Liu, Yuguo, Collerette-Tremblay, Jasmin, Dumontier, Simon, Fabre, Paul, Molina, Thomas, Dort, Junio, Orfi, Zakaria, Denault, Nicolas, Boutin, Joël, Michaud, Joris, Giguère, Hugo, Desroches, Alexandre, Trân, Kien, Ellezam, Benjamin, Vézina, François, Bedard, Sonia, Raynaud, Catherine, Balg, Frederic, Sarret, Philippe, Boudreault, Pierre-Luc, Scott, Michelle S., Denault, Jean-Bernard, Marsault, Eric, Feige, Jerome N., Auger-Messier, Mannix, Dumont, Nicolas A., and Bentzinger, C. Florian

Abstract

Impaired skeletal muscle stem cell (MuSC) function has long been suspected to contribute to the pathogenesis of muscular dystrophy (MD). Here, we showed that defects in the endothelial cell (EC) compartment of the vascular stem cell niche in mouse models of Duchenne MD, laminin α2–related MD, and collagen VI–related myopathy were associated with inefficient mobilization of MuSCs after tissue damage. Using chemoinformatic analysis, we identified the 13–amino acid form of the peptide hormone apelin (AP-13) as a candidate for systemic stimulation of skeletal muscle ECs. Systemic administration of AP-13 using osmotic pumps generated a pro-proliferative EC-rich niche that supported MuSC function through angiocrine factors and markedly improved tissue regeneration and muscle strength in all three dystrophic mouse models. Moreover, EC-specific knockout of the apelin receptor led to regenerative defects that phenocopied key pathological features of MD, including vascular defects, fibrosis, muscle fiber necrosis, impaired MuSC function, and reduced force generation. Together, these studies provide in vivo proof of concept that enhancing endogenous skeletal muscle repair by targeting the vascular niche is a viable therapeutic avenue for MD and characterized AP-13 as a candidate for further study for the systemic treatment of MuSC dysfunction.

Published
2024
Full Text
View/download PDF

23. The adhesion G-protein-coupled receptor Gpr116is essential to maintain the skeletal muscle stem cell pool

Author

Sénéchal, Charlotte, Fujita, Ryo, Jamet, Solène, Maiga, Arhamatoulaye, Dort, Junio, Orfi, Zakaria, Dumont, Nicolas A., Bouvier, Michel, and Crist, Colin

Abstract

Skeletal muscle is populated with a reservoir of quiescent muscle stem cells (MuSCs), which regenerate the tissue after injury. Here, we show that the adhesion G-protein-coupled receptor Gpr116is essential for long-term maintenance of the MuSC pool. Quiescent MuSCs express high levels of Gpr116, which is rapidly downregulated upon MuSC activation. MuSCs deficient for Gpr116exhibit progressive depletion over time and are defective in self-renewal. Adhesion G-protein-coupled receptors contain an agonistic peptide sequence, called the “Stachel” sequence, within their long N-terminal ectodomains. Stimulation of MuSCs with the GPR116 Stachelpeptide delays MuSC activation and differentiation. Stachelpeptide stimulation of GPR116 leads to strong interaction with β-arrestins. Stimulation of GPR116 increases the nuclear localization of β-arrestin1, where it interacts with cAMP response element binding protein to regulate gene expression. Altogether, we propose a model by which GPR116 maintains the MuSC pool via nuclear functions of β-arrestin1.

Published
2022
Full Text
View/download PDF

24. Bi‐allelic variants in MYH3 cause recessively‐inherited arthrogryposis.

Author

Morali, Burcin, Miranda, Valancy, Raelson, John, Grimard, Guy, Glavas, Peter, Audibert, François, Dumont, Nicolas A., Barone, Julia, Bamshad, Michael, Lemyre, Emmanuelle, and Campeau, Philippe M.

Abstract

Arthrogryposis is a clinical feature defined by congenital joint contractures in two or more different body areas which occurs in between 1/3000 and 1/5000 live births. Variants in multiple genes have been associated with distal arthrogryposis syndromes. Heterozygous variants in MYH3 have been identified to cause the dominantly‐inherited distal arthrogryposis conditions, Freeman–Sheldon syndrome, Sheldon–Hall syndrome, and multiple pterygium syndrome. In contrast, MYH3 variants underlie both dominantly and recessively inherited Contractures, Pterygia, and Spondylocarpotarsal Fusion syndromes (CPSFS) which are characterized by extensive bony abnormalities in addition to congenital contractures. Here we report two affected sibs with distal arthrogryposis born to unaffected, distantly related parents. Sequencing revealed that both sibs were homozygous for two ultra‐rare MYH3 variants, c.3445G>A (p.Glu1149Lys) and c.4760T>C (p.Leu1587Pro). Sequencing and deletion/duplication analysis of 169 other arthrogryposis genes yielded no other compelling candidate variants. This is the first report of biallelic variants in MYH3 being implicated in a distal arthrogryposis phenotype without the additional features of CPSFS. Thus, akin to CPSFS, both dominant and recessively inherited distal arthrogryposis can be caused by variants in MYH3. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results