Characterization of a prostaglandin dysfunction myopathy.
Inhibition of prostaglandin synthesis in chicken embryos generated a myopathy characterized by ringbinden, loss of Z disks and thick and thin filaments from the myofibrillar apparatus. During the early stages of myogenesis there was also abnormal clustering and contacts between the developing myotubes. This disruption of myofibrillar apparatus occurred in both primary and secondary myotubes. There was also a slight increase in the proportion of type 1 fibers, which resulted from a selective absence of type 2 fibers. The number of motoneurons in the lumbar spinal cord was normal. This, along with the nature of the disruption of the myofibrillar apparatus, was taken as an indication that the generation of this myopathy was not secondary to abnormal motoneuron development.
D000251:Adenosine Triphosphatases / Q000032:analysis; D000818:Animals; D001241:Aspirin; D002642:Chick Embryo; D007213:Indomethacin; D009046:Motor Neurons / Q000473:pathology; D009132:Muscles / Q000648:ultrastructure; D009135:Muscular Diseases / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D009210:Myofibrils / Q000473:pathology; D011453:Prostaglandins / Q000096:biosynthesis*
D011453:Prostaglandins; D000251:Adenosine Triphosphatases; D001241:Aspirin; D007213:Indomethacin