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NEDD4-1 deficiency impairs satellite cell function during skeletal muscle regeneration.
Cabezas, Felipe; Cabello-Verrugio, Claudio; González, Natalia; Salas, Jeremy; Ramírez, Manuel J; de la Vega, Eduardo; Olguín, Hugo C.
Afiliación
  • Cabezas F; Laboratory of Tissue Repair and Adult Stem Cells, Molecular and Cell Biology Department, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile.
  • Cabello-Verrugio C; Departamento de Ciencias Biológicas y Químicas, Facultad de Medicina y Ciencia, Universidad San Sebastián, Lota 2465, 7510157, Santiago, Chile.
  • González N; Laboratory of Muscle Pathology, Fragility and Aging, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
  • Salas J; Millennium Institute on Immunology and Immunotherapy, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile.
  • Ramírez MJ; Laboratory of Tissue Repair and Adult Stem Cells, Molecular and Cell Biology Department, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile.
  • de la Vega E; Laboratory of Tissue Repair and Adult Stem Cells, Molecular and Cell Biology Department, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile.
  • Olguín HC; Laboratory of Tissue Repair and Adult Stem Cells, Molecular and Cell Biology Department, Faculty of Biological Sciences, Pontificia Universidad Católica de Chile, Santiago, Chile.
Biol Res ; 56(1): 21, 2023 May 05.
Article en En | MEDLINE | ID: mdl-37147738
BACKGROUND: Satellite cells are tissue-specific stem cells primarily responsible for the regenerative capacity of skeletal muscle. Satellite cell function and maintenance are regulated by extrinsic and intrinsic mechanisms, including the ubiquitin-proteasome system, which is key for maintaining protein homeostasis. In this context, it has been shown that ubiquitin-ligase NEDD4-1 targets the transcription factor PAX7 for proteasome-dependent degradation, promoting muscle differentiation in vitro. Nonetheless, whether NEDD4-1 is required for satellite cell function in regenerating muscle remains to be determined. RESULTS: Using conditional gene ablation, we show that NEDD4-1 loss, specifically in the satellite cell population, impairs muscle regeneration resulting in a significant reduction of whole-muscle size. At the cellular level, NEDD4-1-null muscle progenitors exhibit a significant decrease in the ability to proliferate and differentiate, contributing to the formation of myofibers with reduced diameter. CONCLUSIONS: These results indicate that NEDD4-1 expression is critical for proper muscle regeneration in vivo and suggest that it may control satellite cell function at multiple levels.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Músculo Esquelético / Complejo de la Endopetidasa Proteasomal Idioma: En Revista: Biol Res Asunto de la revista: BIOLOGIA Año: 2023 Tipo del documento: Article País de afiliación: Chile Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Músculo Esquelético / Complejo de la Endopetidasa Proteasomal Idioma: En Revista: Biol Res Asunto de la revista: BIOLOGIA Año: 2023 Tipo del documento: Article País de afiliación: Chile Pais de publicación: Reino Unido