scholarly journals Skeletal muscle stem cells adopt a dormant cell state post mortem and retain regenerative capacity

2012 ◽  
Vol 3 (1) ◽  
Author(s):  
Mathilde Latil ◽  
Pierre Rocheteau ◽  
Laurent Châtre ◽  
Serena Sanulli ◽  
Sylvie Mémet ◽  
...  

2018 ◽  
Vol 23 (1) ◽  
pp. 74-85.e6 ◽  
Author(s):  
Sunny Sun-Kin Chan ◽  
Robert W. Arpke ◽  
Antonio Filareto ◽  
Ning Xie ◽  
Matthew P. Pappas ◽  
...  


Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 183 ◽  
Author(s):  
David Lee ◽  
Akshay Bareja ◽  
David Bartlett ◽  
James White

Skeletal muscle has remarkable regenerative capacity, relying on precise coordination between resident muscle stem cells (satellite cells) and the immune system. The age-related decline in skeletal muscle regenerative capacity contributes to the onset of sarcopenia, prolonged hospitalization, and loss of autonomy. Although several age-sensitive pathways have been identified, further investigation is needed to define targets of cellular dysfunction. Autophagy, a process of cellular catabolism, is emerging as a key regulator of muscle regeneration affecting stem cell, immune cell, and myofiber function. Muscle stem cell senescence is associated with a suppression of autophagy during key phases of the regenerative program. Macrophages, a key immune cell involved in muscle repair, also rely on autophagy to aid in tissue repair. This review will focus on the role of autophagy in various aspects of the regenerative program, including adult skeletal muscle stem cells, monocytes/macrophages, and corresponding age-associated dysfunction. Furthermore, we will highlight rejuvenation strategies that alter autophagy to improve muscle regenerative function.



2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jinhong Meng ◽  
Maximilien Bencze ◽  
Rowan Asfahani ◽  
Francesco Muntoni ◽  
Jennifer E Morgan


2017 ◽  
Author(s):  
Natalia Pietrosemoli ◽  
Sébastien Mella ◽  
Siham Yennek ◽  
Meryem B. Baghdadi ◽  
Hiroshi Sakai ◽  
...  

AbstractBackgroundSkeletal muscle stem cells (MuSCs) are quiescent in adult mice and can undergo multiple rounds of proliferation and self-renewal following muscle injury. Several labs have profiled transcripts of myogenic cells during developmental and adult myogenesis with the aim of identifying quiescent markers. Here, we focused on the quiescent cell state and generated new transcriptome profiles that include subfractionations of adult MuSC populations, and an artificially induced prenatal quiescent state, to identify core signatures for quiescent and proliferating MuSCs.MethodsComparison of available data offered challenges related to the inherent diversity of datasets and biological conditions. We developed a standardized workflow to homogenize the normalization, filtering, quality control steps for the analysis of gene expression profiles allowing the identification up- and down-regulated genes and the subsequent gene set enrichment analysis. To share the analytical pipeline of this work, we developed Sherpa, an interactive Shiny server that allows multiscale comparisons for extraction of desired gene sets from the analysed datasets. This tool is adaptable to cell populations in other contexts and tissues.ResultsA multiscale analysis comprising eight datasets of quiescent MuSCs had 207 and 542 genes commonly up- and down-regulated, respectively. Shared up-regulated gene sets include an over-representation of the TNFa pathway via NFKb signaling, Il6-Jak-Stat3 signaling, and the apical surface processes, while shared down-regulated gene sets exhibited an over-representation of Myc and E2F targets, and genes associated to the G2M checkpoint and oxidative phosphorylation. However, virtually all datasets contained genes that are associated with activation or cell cycle entry, such as the immediate early stress response genes Fos and Jun. Empirical examination of fixed and isolated MuSCs showed that these and other genes were absent in vivo, but activated during procedural isolation of cells.ConclusionsThrough the systematic comparison and individual analysis of diverse transcriptomic profiles, we identified genes that were consistently differentially expressed among the different datasets and common underlying biological processes key to the quiescent cell state. Our findings provide impetus to define and distinguish transcripts associated with true in vivo quiescence from those that are first responding genes due to disruption of the stem cell niche.



2014 ◽  
Vol 146 (5) ◽  
pp. S-158
Author(s):  
Johanna G. Palmadottir ◽  
Anu Maharjan ◽  
Andrew Draghi ◽  
Francisco A. Sylvester ◽  
Morgan E. Carlson


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