Apoptosis and repair of denervated muscle

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The purpose of this study is to examined the cellular and molecular events coincident with muscle denervation, especially a regenerative change seen following muscle denervation, the role of satellite cells involved in the process, and the possibility of apoptotic degeneration of myonuclei as a mechanism of myonuclei loss during muscle denervation atrophy. Myosin heavy chain (MHC) isoform expression during muscle denervation was examined using pyrophosphate acrylamide gel electrophoresis and immunohistochemistry. DNA fragmentation (apoptosis) in myonuclei of denervated fibers was investigated using agarose gel electrophoresis, the TUNEL technique and ELISA.Immunohistchemistry for MyoD and BrdU,and an ultrastructural survey were also performed. Following muscle denervation, embryonic MHC which is not expressed in adult healthy muscles was expressed in some denervated fibers as well as small activated satellite cells ; maximal expression was observed two to three weeks after denervation. Activation and proliferation of satellite cells were observed, while few typical regenerating fibers were identified, suggesting that activated satellite cells fused to the denervated maternal fibers to try to repair them instead of fusing to each other to form ner fibers, likely as a mechanism to compensate for atrophic changes after denervation. DNA fragmentation was detected by the TUNEL technique and ELISA,although DNA ladder formation was not observed with agarose gel electrophoresis. Apoptotic degeneration of myonuclei of denervated fibers was not confirmed, but it may contribute to loss of myoneuclei associated with denervation atrophy and induce activation of satellite cells.