[Apoptosis in atrophic skeletal muscle induced by brachial plexus injury in rats].
OBJECTIVE
To study the role of apoptosis and the expression of apoptosis-associated genes in skeletal muscle atrophy induced by brachial plexus injury in rats.


METHODS
Rat models of skeletal muscle atrophy were established by cutting off brachial plexus of one upper limb. Apoptosis of muscular cells was investigated by TUNEL, flowcytometry, DNA electrophoresis and electromicroscopic observation. The apoptosis associated genes such as Fas, FADD, Caspase 8, c-myc, P53 and Bcl-2 were detected by immunohistochemical method (ABC) and Northern-blot.


RESULTS
It was found with TUNEL and flowcytometry that the percentage of apoptotic muscle cell rose obviously in atrophic skeletal muscle (P < 0.05). DNA laddering could be seen in DNA gel electrophoresis of atrophic muscle after brachial injury. Morphologic changes of early stage in apoptotic cell could be seen under eletcromicroscope, such as the aggregation of chromosome, the expansion of nucleic cistern and the contraction of nucleus. Fas, FADD and Caspase genes were expressed highly and Bcl-2 gene was expressed lowly with immunohistochemical method in atrophic muscle. The results were all significantly different with that of the controls (P < 0.01). But the expression changes in P53 and c-myc genes were not obvious. The result of Northern-blot indicated that the mRNA of Fas gene rose and that of Bcl-2 gene decreased obviously (P < 0.01) in atrophic muscle induced by brachial plexus injury.


CONCLUSIONS
There are much more apoptotic cells in atrophic muscle induced by brachial plexus injury, and apoptosis plays an important role in its pathogenesis. The apoptotic signal maybe transmitted through Fas-->FADD-->Caspase 8, and the decrease in Bcl-2 gene expression aggravates the process.
Tian
T
T
Department of Pathophysiology, Shanghai Medical University, Shanghai 200032, China.
Wu
Z
Z
Jin
H
H
D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D017209:Apoptosis; D015152:Blotting, Northern; D001917:Brachial Plexus / Q000293:injuries*; D002352:Carrier Proteins / Q000032:analysis; D053181:Caspase 8; D053453:Caspase 9; D020169:Caspases / Q000032:analysis; D053200:Fas-Associated Death Domain Protein; D007150:Immunohistochemistry; D008854:Microscopy, Electron; D018482:Muscle, Skeletal / Q000737:chemistry / Q000473:pathology* / Q000648:ultrastructure; D009133:Muscular Atrophy / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis / Q000235:genetics; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000235:genetics; D016271:Proto-Oncogene Proteins c-myc / Q000032:analysis; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
D048868:Adaptor Proteins, Signal Transducing; D002352:Carrier Proteins; C505535:Fadd protein, rat; D053200:Fas-Associated Death Domain Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D016760:Proto-Oncogene Proteins c-fos; D016271:Proto-Oncogene Proteins c-myc; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; C505528:Casp8 protein, rat; C506435:Casp9 protein, rat; D053181:Caspase 8; D053453:Caspase 9; D020169:Caspases