Unbound MEDLINE

Inhibition of prostaglandin synthesis reduces the induction of MyoD expression in rat soleus muscle. Journal of muscle research and cell motility [J Muscle Res Cell Motil] Journal article

 
TitleInhibition of prostaglandin synthesis reduces the induction of MyoD expression in rat soleus muscle.
Author(s)Monda M, Vicidomini C, Viggiano A, Sampaolo S, Di Iorio G, Viggiano A, Viggiano E, De Luca B 
InstitutionDepartment of Experimental Medicine, Section of Human Physiology, Second University of Naples, Via Costantinopoli 16, 80138, Naples, Italy, marcellino.monda@unina2.it.
SourceJ Muscle Res Cell Motil 2009 Jun 13.
AbstractMyoD is a myogenic regulatory factor with a critical role in skeletal muscle development and regeneration. As muscle regeneration comes with an inflammatory process, it has been proposed that the inflammatory cells can play an important role in the induction of muscle fibres regeneration. The aim of the present work was to verify if a cyclooxygenase inhibitory drug (ketoprofen) would alter the normal expression of MyoD in a regenerating rat soleus muscle after an over-load lesion. Using immunohistochemical techniques, the numbers of m-cadherin-positive cells, a selective marker of satellite cells, and MyoD-positive cells were evaluated in functionally overloaded rat soleus muscles 4 days after a gastrocnemius tendon cut. The same study was conducted either with four rats injected with ketoprofen (100 mg/kg b.w./day) or with four rats injected with saline solution. The data obtained showed a very large decrease in the number of MyoD positive/m-cadherin positive cells in the ketoprofen injected group compared to the control group. Although further studies are needed to elucidate the sequence of biochemical events that induce a reduction of MyoD expression due to ketoprofen, the results demonstrate that prostaglandin synthesis is required for the induction of MyoD expression and that ketoprofen can affect this expression, with possible adverse effects on muscle regeneration.
LanguageENG
Pub Type(s)JOURNAL ARTICLE
PubMed ID19526318