Characterization of a myopathy caused by prostaglandin dysfunction.
Administration of inhibitors of prostaglandin synthetase to chicken embryos produced myopathies in their skeletal muscles which were characterized by ringbinden, loss of Z-discs, M-bands, and thick and thin filaments and decreased myoblast proliferation and type 2 myotube formation. The effect of administration of prostaglandins on myoblast proliferation was also examined and PGE was found to suppress proliferation. There was also a tendency for PGF2 alpha to suppress and PGI2 to stimulate proliferation, although neither of these effects were statistically significant. PGA, PGB and PGD did not affect myoblast proliferation.
McLennan
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Department of Behavioural Biology, Research School of Biological Sciences, Australian National University, Canberra.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D002642:Chick Embryo; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D009132:Muscles / Q000473:pathology; D009136:Muscular Dystrophies / Q000503:physiopathology*; D009137:Muscular Dystrophy, Animal / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000502:physiology
D011453:Prostaglandins; D011458:Prostaglandins E; D000251:Adenosine Triphosphatases; D001241:Aspirin; D007213:Indomethacin