دورية أكاديمية

miR-106b is a novel target to promote muscle regeneration and restore satellite stem cell function in injured Duchenne dystrophic muscle

التفاصيل البيبلوغرافية
العنوان: miR-106b is a novel target to promote muscle regeneration and restore satellite stem cell function in injured Duchenne dystrophic muscle
المؤلفون: Lara Rodriguez-Outeiriño, Francisco Hernandez-Torres, Felicitas Ramirez de Acuña, Alberto Rastrojo, Carlota Creus, Alejandra Carvajal, Luis Salmeron, Marisol Montolio, Patricia Soblechero-Martin, Virginia Arechavala-Gomeza, Diego Franco, Amelia Eva Aranega
المصدر: Molecular Therapy: Nucleic Acids, Vol 29, Iss , Pp 769-786 (2022)
بيانات النشر: Elsevier
سنة النشر: 2022
المجموعة: Directory of Open Access Journals: DOAJ Articles
مصطلحات موضوعية: MT: Non-coding RNAs, satellite cell, miR-106b, stemness, muscle regeneration, muscular dystrophy, Therapeutics. Pharmacology, RM1-950
الوصف: Satellite cells (SCs), muscle stem cells, display functional heterogeneity, and dramatic changes linked to their regenerative capabilities are associated with muscle-wasting diseases. SC behavior is related to endogenous expression of the myogenic transcription factor MYF5 and the propensity to enter into the cell cycle. Here, we report a role for miR-106b reinforcing MYF5 inhibition and blocking cell proliferation in a subset of highly quiescent SC population. miR-106b down-regulation occurs during SC activation and is required for proper muscle repair. In addition, miR-106b is increased in dystrophic mice, and intramuscular injection of antimiR in injured mdx mice enhances muscle regeneration promoting transcriptional changes involved in skeletal muscle differentiation. miR-106b inhibition promotes the engraftment of human muscle stem cells. Furthermore, miR-106b is also high in human dystrophic muscle stem cells and its inhibition improves intrinsic proliferative defects and increases their myogenic potential. This study demonstrates that miR-106b is an important modulator of SC quiescence, and that miR-106b may be a new target to develop therapeutic strategies to promote muscle regeneration improving the regenerative capabilities of injured dystrophic muscle.
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 2162-2531
العلاقة: http://www.sciencedirect.com/science/article/pii/S2162253122002244Test; https://doaj.org/toc/2162-2531Test; https://doaj.org/article/e03b3b8ff3f848cdb79d4103a8b2c6f8Test
DOI: 10.1016/j.omtn.2022.08.025
الإتاحة: https://doi.org/10.1016/j.omtn.2022.08.025Test
https://doaj.org/article/e03b3b8ff3f848cdb79d4103a8b2c6f8Test
رقم الانضمام: edsbas.F0FE931
قاعدة البيانات: BASE
الوصف
تدمد:21622531
DOI:10.1016/j.omtn.2022.08.025