Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2006; Volume 186, Supplement 650
Joint Meeting of The German Society of Physiology and The Federation of European Physiological Societies 2006
3/26/2006-3/29/2006
Ludwig-Maximilians-University, Munich


PROSTAGLANDIN SYNTHESIS IS INVOLVED IN THE INDUCTION OF MYOD EXPRESSION
Abstract number: PT04A-13

Viggiano1 A, Vicidomini1 C, Sampaolo2 S, Di Iorio2 G, Monda2 M, Viggiano2 E, Viggiano2 A, De Luca2 B

1Second University of Naples, Dept. Experimental Medicine Human Physiology
2Dept. Neurological Sciences

MyoD 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 (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 on 4 rats injected with ketoprofen (3mg/Kg b.w./day) and 4 rats injected with saline. The data obtained showed a very large decrease in the ratio MyoD positive/m-cadherin positive cells in the ketoprofen injected group compared to the control group. This result demonstrates that the prostaglandin synthesis is required for the induction of MyoD expression and that ketoprofen can modify the normal sequence of regulatory genes activation. Further studies are needed to elucidate possible adverse or positive effects of such drug intervention on the muscle fiber regeneration.

To cite this abstract, please use the following information:
Acta Physiologica 2006; Volume 186, Supplement 650 :PT04A-13

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE