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1 Growth and Development Laboratory, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, United States; Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
2 Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
3 Growth and Development Laboratory, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, United States; Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
4 Growth and Development Laboratory, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, United States
5 Growth and Development Laboratory, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, United States; Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States; Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: jhuard{at}pitt.edu.
Non-steroidal 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 F2
(PGF2) 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 that PGE2 and PGF2had on cell fusion. For the in vivo experiments, we created a 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 healing histologically and physiologically. We found that the secondary fusion between nascent myotubes and myogenic precursor cells isolated from COX-2-/- mice was compromised when compared with that of Wt controls, but was restored by the addition of PGF2 or, to a lesser extent, PGE2 to the culture. Histological and physiological 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. Our results indicate 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.
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