The genotype of bone marrow-derived inflammatory cells does not account for differences in skeletal muscle regeneration between SJL/J and BALB/c mice

1995 ◽  
Vol 280 (2) ◽  
pp. 407-413 ◽  
Author(s):  
Christopher A. Mitchell ◽  
Miranda D. Grounds ◽  
John M. Papadimitriou
PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e37656 ◽  
Author(s):  
Yan Gao ◽  
Yanfeng Li ◽  
Xing Guo ◽  
Zhenguo Wu ◽  
Wei Zhang

2004 ◽  
Vol 287 (2) ◽  
pp. C475-C483 ◽  
Author(s):  
Brenda A. Bondesen ◽  
Stephen T. Mills ◽  
Kristy M. Kegley ◽  
Grace K. Pavlath

Skeletal muscle regeneration comprises several overlapping cellular processes, including inflammation and myogenesis. Prostaglandins (PGs) may regulate muscle regeneration, because they modulate inflammation and are involved in various stages of myogenesis in vitro. PG synthesis is catalyzed by different isoforms of cyclooxygenase (COX), which are inhibited by nonsteroidal anti-inflammatory drugs. Although experiments employing nonsteroidal anti-inflammatory drugs have implicated PGs in tissue repair, how PGs regulate muscle regeneration remains unclear, and the potentially distinct roles of different COX isoforms have not been investigated. To address these questions, a localized freeze injury was induced in the tibialis anterior muscles of mice chronically treated with either a COX-1- or COX-2-selective inhibitor (SC-560 and SC-236, respectively), starting before injury. The size of regenerating myofibers was analyzed at time points up to 5 wk after injury and found to be decreased by SC-236 and in COX-2−/− muscles, but unaffected by SC-560. In contrast, SC-236 had no effect on myofiber growth when administered starting 7 days after injury. The attenuation of myofiber growth by SC-236 treatment and in COX-2−/− muscles is associated with decreases in the number of myoblasts and intramuscular inflammatory cells at early times after injury. Together, these data suggest that COX-2-dependent PG synthesis is required during early stages of muscle regeneration and thus raise caution about the use of COX-2-selective inhibitors in patients with muscle injury or disease.


2008 ◽  
Vol 23 (2) ◽  
pp. 382-395 ◽  
Author(s):  
Dongxu Sun ◽  
Carlo O. Martinez ◽  
Oscar Ochoa ◽  
Lourdes Ruiz‐Willhite ◽  
Jose R. Bonilla ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-20 ◽  
Author(s):  
Junio Dort ◽  
Paul Fabre ◽  
Thomas Molina ◽  
Nicolas A. Dumont

Muscle regeneration is a closely regulated process that involves a variety of cell types such as satellite cells, myofibers, fibroadipogenic progenitors, endothelial cells, and inflammatory cells. Among these different cell types, macrophages emerged as a central actor coordinating the different cellular interactions and biological processes. Particularly, the transition of macrophages from their proinflammatory to their anti-inflammatory phenotype was shown to regulate inflammation, myogenesis, fibrosis, vascularization, and return to homeostasis. On the other hand, deregulation of macrophage accumulation or polarization in chronic degenerative muscle disorders was shown to impair muscle regeneration. Considering the key roles of macrophages in skeletal muscle, they represent an attractive target for new therapeutic approaches aiming at mitigating various muscle disorders. This review aims at summarizing the novel insights into macrophage heterogeneity, plasticity, and functions in skeletal muscle homeostasis, regeneration, and disease.


2011 ◽  
Vol 20 (2) ◽  
pp. 217-232 ◽  
Author(s):  
Anabel S. De La Garza-Rodea ◽  
Ietje Van Der Velde ◽  
Hester Boersma ◽  
Manuel A. F. V. Gonçalves ◽  
Dirk W. Van Bekkum ◽  
...  

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