Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 214, Issue 2, Pages 405-412Publisher
WILEY-LISS
DOI: 10.1002/jcp.21212
Keywords
-
Categories
Funding
- NCRR NIH HHS [C06 RR-14489] Funding Source: Medline
- NIAMS NIH HHS [1R01 AR 47973-01] Funding Source: Medline
Ask authors/readers for more resources
Inflammation, an important phase of skeletal muscle healing, largely involves macrophages, TGF-beta 1, and the COX-2 pathway. To improve our understanding of how these molecules interact during all phases of muscle healing, we examined their roles in muscle cells in vitro and in vivo. Initially, we found that depletion of macrophages in muscle tissue led to reduced muscle regeneration. Macrophages may influence healing by inducing the production of TGF-beta 1 and PGE(2) in different muscle cell types. We then found that the addition of TGF-beta 1 induced PGE(2) production in muscle cells, an effect probably mediated by COX-2 enzyme. It was also found that TGF-beta 1 enhanced macrophage infiltration in wild-type mice after muscle injury. However, this effect was not observed in COX-2(-/-) mice, suggesting that the effect of TGF-beta 1 on macrophage infiltration is mediated by the COX-2 pathway. Furthermore, we found that PGE(2) can inhibit the expression of TGF-beta 1. PGE2 and TGF-beta 1 may be involved in a negative feedback loop balancing the level of fibrosis formation during skeletal muscle healing. In conclusion, our results suggest a complex regulatory mechanism of skeletal muscle healing. Macrophages, TGF-beta 1, and the COX-2 pathway products may regulate one another's levels and have profound influence on the whole muscle healing process.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available