%0 Journal Article
%A Rodriguez-Outeiriño, Lara
%A Hernandez-Torres, Francisco
%A Ramirez de Acuña, Felicitas
%A Rastrojo, Alberto
%A Creus, Carlota
%A Carvajal, Alejandra
%A Salmeron, Luis
%A Montolio, Marisol
%A Soblechero-Martin, Patricia
%A Arechavala-Gomeza, Virginia
%A Franco, Diego
%A Aranega, Amelia Eva
%T miR-106b is a novel target to promote muscle regeneration and restore satellite stem cell function in injured Duchenne dystrophic muscle.
%D 2022
%@ 2162-2531
%U http://hdl.handle.net/10668/22463
%X 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.
%K MT: Non-coding RNAs
%K miR-106b
%K muscle regeneration
%K muscular dystrophy
%K satellite cell
%K stemness
%~