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Inhibited skeletal muscle healing in cyclooxygenase-2 gene-deficient mice: The role of PGE<inf>2</inf> and PGF<inf>2α</inf>

Shen, W and Prisk, V and Li, Y and Foster, W and Huard, J (2006) Inhibited skeletal muscle healing in cyclooxygenase-2 gene-deficient mice: The role of PGE<inf>2</inf> and PGF<inf>2α</inf>. Journal of Applied Physiology, 101 (4). 1215 - 1221. ISSN 8750-7587

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat skeletal muscle injury. However, studies have shown that NSAIDs may be detrimental to the healing process. Mediated by prostaglandin F 2α (PGF2α) and prostaglandin E2 (PGE2), the cycloxygenase-2 (COX-2) pathway plays an important role in muscle healing. We hypothesize that the COX-2 pathway is important for the fusion of muscle cells and the regeneration of injured muscle. For the in vitro experiments, we isolated myogenic precursor cells from wild-type (Wt) and COX-2 gene-deficient (COX-2-/-) mice and examined the effect of PGE 2 and PGF2α on cell fusion. For the in vivo experiments, we created laceration injury on the tibialis anterior (TA) muscles of Wt and COX-2-/- mice. Five and 14 days after injury, we examined the TA muscles histologically and functionally. We found that the secondary fusion between nascent myotubes and myogenic precursor cells isolated from COX-2-/- mice was severely compromised compared with that of Wt controls but was restored by the addition of PGF2α or, to a lesser extent, PGE2 to the culture. Histological and functional assessments of the TA muscles in COX-2-/- mice revealed decreased regeneration relative to that observed in the Wt mice. The findings reported here demonstrate that the COX-2 pathway plays an important role in muscle healing and that prostaglandins are key mediators of the COX-2 pathway. It suggests that the decision to use NSAIDs to treat muscle injuries warrants critical evaluation because NSAIDs might impair muscle healing by inhibiting the fusion of myogenic precursor cells. Copyright © 2006 the American Physiological Society.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Shen, W
Prisk, V
Li, Y
Foster, W
Huard, J
Date: 9 October 2006
Date Type: Publication
Journal or Publication Title: Journal of Applied Physiology
Volume: 101
Number: 4
Page Range: 1215 - 1221
DOI or Unique Handle: 10.1152/japplphysiol.01331.2005
Schools and Programs: School of Medicine > Biochemistry and Molecular Genetics
School of Medicine > Orthopaedic Surgery
Swanson School of Engineering > Bioengineering
Refereed: Yes
ISSN: 8750-7587
MeSH Headings: Animals; Cell Fusion; Cell Movement--drug effects; Cell Survival--drug effects; Cells, Cultured; Cyclooxygenase 2--deficiency; Cyclooxygenase 2--genetics; Dinoprost--pharmacology; Dinoprostone--pharmacology; Dose-Response Relationship, Drug; Mice; Mice, Knockout; Muscle Fibers, Skeletal--drug effects; Muscle Fibers, Skeletal--metabolism; Muscle Fibers, Skeletal--pathology; Muscle, Skeletal--drug effects; Muscle, Skeletal--metabolism; Muscle, Skeletal--pathology; Myoblasts--drug effects; Myoblasts--metabolism; Myoblasts--pathology; Wound Healing--drug effects; Wound Healing--physiology
PubMed ID: 16778000
Date Deposited: 09 Jun 2014 14:46
Last Modified: 11 Jun 2021 22:55


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