Objective: After the injury of adult mammal animal central nerve systems, many factors inbibit the regeneration, among which oligodendrocyte and myelin associated inhibitors are important. They inhibit axon regeneration through combination with common receptor Nogo-66. Recently, we have also found that there are different receptor approaches with Nogo-A, myelin associated glucoprotein (MAG), and these have provided new ways for later research of regeneration after central nervous system (CNS) injury. This text is aimed to review the research development of Nogo-A, MAG, oligodendrocyte myelin glycoprotein (OMgp) and its receptors. Data Sources: We searched the PUBMED database for related articles with the key words of "Nogo-A, MAG, OMgp, NgR" published from January 1981 to May 2004 in English. Study Selection: The literatures of rat model for CNS injury were selected firstly, and those were not about the study of animal model were deleted, and then the full-texts of the rest ones were searched. Whether these included randomized animal models experiments or not were judged further. Inclusive criteria: (1)the randomized experiments of animal models, no matter single blind, double blind or non-blind trials; (2)the parallel-control groups included un-treated or healthy animal models. Treatment group contained animal models with CNS injury. Exclusive criteria: those were obviously non-randomized research or non-animal model research. Evaluation: the facticity of the material, the rationality of the experiments, the exactness of the observation and tests, the stringency of the statistics; repetitive research or Meta analysis articles. Data Extraction: Totally 30 related articles were collected. Of the 6 excluded articles, 2 ones were duplicated researches, 4 ones were not rat-models. Totally 24 articles were accorded with the inclusive criteria, of which 7 papers were related to Nogo-A, 8 papers were related to MAG, 5 papers were related to OMgp, 5 papers were related to Nogo-66 receptor and others. Data Synthesis: Nogo-A included Nogo-66 and amino-Nogo functional structural domains, which had inhibitory effect on axon growth. MAG not only could inhibit adult axon growth, but also promote the growth of new axon. OMgp, a glycosyl-phosphatidyl inositol anchor protein, was rich in leucine repeated segments, participated in interaction among protein, had the function of DNA repair, RNA splicing, cell adhesion, signal transduction and so on. Conclusion: Various factors inhibit axon regeneration through combination with common receptors in adult mammalian after CNS injury. These have provided basis for later research of regeneration after CNS injury.
|Original language||English (US)|
|Number of pages||3|
|Journal||Chinese Journal of Clinical Rehabilitation|
|State||Published - Oct 10 2006|
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