Loss of HDAC11 accelerates skeletal muscle regeneration in mice
| Autor: | Erica Hurtado, Miguel A. Peinado, Lauro Sumoy, Yaiza Núñez-Álvarez, Raquel Pluvinet, Gabriel E. Rech, Ignacio García-Tuñón, Mar Muñoz, Alberto M. Pendás, Mònica Suelves |
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| Přispěvatelé: | Ministerio de Economía y Competitividad (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia, Innovación y Universidades (España), Generalitat de Catalunya, Junta de Castilla y León, European Commission |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Satellite Cells Skeletal Muscle Population Biology Muscle Development Biochemistry Histone Deacetylases Cell Line Muscle hypertrophy 03 medical and health sciences 0302 clinical medicine Satellite cells Skeletal muscle regeneration HDAC11 medicine Animals Humans Regeneration Myocyte RNA-Seq Muscle Skeletal education Molecular Biology Cells Cultured Cell Proliferation Cell cycle exit Mice Knockout education.field_of_study Gene Expression Profiling Regeneration (biology) Skeletal muscle Cell Differentiation Cell Biology Cell biology 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis IL-10 Stem cell Cell activation |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname |
| ISSN: | 1742-4658 1742-464X |
| Popis: | Histone deacetylase 11 (HDAC11) is the latest identified member of the histone deacetylase family of enzymes. It is highly expressed in brain, heart, testis, kidney, and skeletal muscle, although its role in these tissues is poorly understood. Here, we investigate for the first time the consequences of HDAC11 genetic impairment on skeletal muscle regeneration, a process principally dependent on its resident stem cells (satellite cells) in coordination with infiltrating immune cells and stromal cells. Our results show that HDAC11 is dispensable for adult muscle growth and establishment of the satellite cell population, while HDAC11 deficiency advances the regeneration process in response to muscle injury. This effect is not caused by differences in satellite cell activation or proliferation upon injury, but rather by an enhanced capacity of satellite cells to differentiate at early regeneration stages in the absence of HDAC11. Infiltrating HDAC11‐deficient macrophages could also contribute to this accelerated muscle regenerative process by prematurely producing high levels of IL‐10, a cytokine known to promote myoblast differentiation. Altogether, our results show that HDAC11 depletion advances skeletal muscle regeneration and this finding may have potential implications for designing new strategies for muscle pathologies coursing with chronic damage. This work was supported by Ministerio de Economía y Competitividad (BFU2016‐80748 to MS and BFU2017‐89408‐R to AMP) and Ministerio de Ciencia, Innovación y Universidades (RTI2018‐094009‐B‐I00 to MAP), FEDER funds, Generalitat de Catalunya (2017 SGR969 and 2017 SGR206), and Junta de Castilla y Leon (CSI239P18). YN‐A was supported by FPU12/05668, and EH was supported in part by BFU2016‐80748 project. |
| Databáze: | OpenAIRE |
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