Injury-Induced Senescence Enables In Vivo Reprogramming in Skeletal Muscle
| Autor: | Han Li, Patricia Flamant, Shahragim Tajbakhsh, Olinda Alegria, Coralie Cazin, Sabela Búa Aguín, Hiroshi Sakai, Laurence Fiette, Rana Salam, Isabelle Roux, Aurélie Chiche, Mathieu von Joest |
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| Přispěvatelé: | Plasticité cellulaire et Modélisation des Maladies / Cellular Plasticity and Disease Modelling, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Cellules Souches et Développement / Stem Cells and Development, Histopathologie humaine et Modèles animaux, Institut Pasteur [Paris] (IP), LI, HAN |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Senescence [SDV]Life Sciences [q-bio] cellular plasticity Biology 03 medical and health sciences Paracrine signalling Genetics medicine Animals skeletal muscle Interleukin 6 Muscle Skeletal Cellular Senescence IL-6 Stem Cells aging Skeletal muscle Cell Biology pluripotency Cellular Reprogramming Phenotype Cell biology [SDV] Life Sciences [q-bio] Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure regeneration in vivo reprogramming biology.protein Molecular Medicine PAX7 Stem cell Reprogramming |
| Zdroj: | Cell Stem Cell Cell Stem Cell, 2017, 20 (3), pp.407-414.e4. ⟨10.1016/j.stem.2016.11.020⟩ |
| ISSN: | 1875-9777 1934-5909 |
| DOI: | 10.1016/j.stem.2016.11.020⟩ |
| Popis: | International audience; In vivo reprogramming is a promising approach for tissue regeneration in response to injury. Several examples of in vivo reprogramming have been reported in a variety of lineages, but some including skeletal muscle have so far proven refractory. Here, we show that acute and chronic injury enables transcription-factor-mediated reprogramming in skeletal muscle. Lineage tracing indicates that this response frequently originates from Pax7+ muscle stem cells. Injury is associated with accumulation of senescent cells, and advanced aging or local irradiation further enhanced in vivo reprogramming, while selective elimination of senescent cells reduced reprogramming efficiency. The effect of senescence appears to be, at least in part, due to the release of interleukin 6 (IL-6), suggesting a potential link with the senescence-associated secretory phenotype. Collectively, our findings highlight a beneficial paracrine effect of injury-induced senescence on cellular plasticity, which will be important for devising strategies for reprogramming-based tissue repair. |
| Databáze: | OpenAIRE |
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