JMJD3 activated hyaluronan synthesis drives muscle regeneration in an inflammatory environment.

Autor:	Nakka K; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada., Hachmer S; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada., Mokhtari Z; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada., Kovac R; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada., Bandukwala H; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada., Bernard C; Institut NeuroMyoGène, Unité Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, CNRS 5261, INSERM U1315, Université de Lyon, Lyon, France., Li Y; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada., Xie G; National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA., Liu C; Transgenic Core, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA., Fallahi M; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada., Megeney LA; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada., Gondin J; Institut NeuroMyoGène, Unité Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, CNRS 5261, INSERM U1315, Université de Lyon, Lyon, France., Chazaud B; Institut NeuroMyoGène, Unité Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, CNRS 5261, INSERM U1315, Université de Lyon, Lyon, France., Brand M; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.; LIFE Research Institute, University of Ottawa, Ottawa, ON, Canada., Zha X; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada., Ge K; National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA., Dilworth FJ; Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada.; Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.; LIFE Research Institute, University of Ottawa, Ottawa, ON, Canada.
Jazyk:	angličtina
Zdroj:	Science (New York, N.Y.) [Science] 2022 Aug 05; Vol. 377 (6606), pp. 666-669. Date of Electronic Publication: 2022 Aug 04.
DOI:	10.1126/science.abm9735
Abstrakt:	Muscle stem cells (MuSCs) reside in a specialized niche that ensures their regenerative capacity. Although we know that innate immune cells infiltrate the niche in response to injury, it remains unclear how MuSCs adapt to this altered environment for initiating repair. Here, we demonstrate that inflammatory cytokine signaling from the regenerative niche impairs the ability of quiescent MuSCs to reenter the cell cycle. The histone H3 lysine 27 (H3K27) demethylase JMJD3, but not UTX, allowed MuSCs to overcome inhibitory inflammation signaling by removing trimethylated H3K27 (H3K27me3) marks at the Has2 locus to initiate production of hyaluronic acid, which in turn established an extracellular matrix competent for integrating signals that direct MuSCs to exit quiescence. Thus, JMJD3-driven hyaluronic acid synthesis plays a proregenerative role that allows MuSC adaptation to inflammation and the initiation of muscle repair.
Databáze:	MEDLINE
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