Link to the University of Pittsburgh Homepage
Link to the University Library System Homepage Link to the Contact Us Form

Interaction between macrophages, TGF-β1, and the COX-2 pathway during the inflammatory phase of skeletal muscle healing after injury

Shen, W and Li, Y and Zhu, J and Schwendener, R and Huard, J (2008) Interaction between macrophages, TGF-β1, and the COX-2 pathway during the inflammatory phase of skeletal muscle healing after injury. Journal of Cellular Physiology, 214 (2). 405 - 412. ISSN 0021-9541

[img] Plain Text (licence)
Available under License : See the attached license file.

Download (1kB)


Inflammation, an important phase of skeletal muscle healing, largely involves macrophages, TGF-β1, 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-β1 and PGE2 in different muscle cell types. We then found that the addition of TGF-β1 induced PGE2 production in muscle cells, an effect probably mediated by COX-2 enzyme. It was also found that TGF-β1 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-β1 on macrophage infiltration is mediated by the COX-2 pathway. Furthermore, we found that PGE2 can inhibit the expression of TGF-β1. PGE2 and TGF-β1 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-β1, and the COX-2 pathway products may regulate one another's levels and have profound influence on the whole muscle healing process. © 2007 Wiley-Liss, Inc.


Social Networking:
Share |


Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Shen, W
Li, Y
Zhu, J
Schwendener, R
Huard, J
Centers: Other Centers, Institutes, Offices, or Units > Stem Cell Research Center
Date: 1 February 2008
Date Type: Publication
Journal or Publication Title: Journal of Cellular Physiology
Volume: 214
Number: 2
Page Range: 405 - 412
DOI or Unique Handle: 10.1002/jcp.21212
Schools and Programs: School of Medicine > Orthopaedic Surgery
Swanson School of Engineering > Bioengineering
Refereed: Yes
ISSN: 0021-9541
MeSH Headings: Animals; Cardiotoxins--administration & dosage; Cells, Cultured; Clodronic Acid--administration & dosage; Cyclooxygenase 2--genetics; Cyclooxygenase 2--metabolism; Dinoprostone--pharmacology; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Histocytochemistry; Inflammation--chemically induced; Inflammation--metabolism; Liposomes; Macrophages, Peritoneal--metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Muscle, Skeletal--cytology; Muscle, Skeletal--injuries; Muscle, Skeletal--metabolism; Muscle, Skeletal--physiology; Regeneration--drug effects; Regeneration--physiology; Transforming Growth Factor beta1--antagonists & inhibitors; Transforming Growth Factor beta1--metabolism
PubMed ID: 17657727
Date Deposited: 15 May 2014 20:29
Last Modified: 11 Jun 2021 22:55


Monthly Views for the past 3 years

Plum Analytics

Actions (login required)

View Item View Item