title: Gene expression profiling reveals multiple novel intrinsic and extrinsic factors associated with axonal regeneration failure.
abstract: In contrast to the regeneration-competent peripheral nervous system (PNS), lesions of nerve tracts within the central nervous system (CNS) lead to chronically impaired neuronal connections. We have analysed changes in gene expression patterns occurring as a consequence of postcommissural fornix transection at a time when spontaneous axonal growth has ceased at the lesion site. This was done in order to describe both extrinsic and intrinsic determinants of regeneration failure. Using a genomic approach we have identified a number of so far undetected factors such as bamacan and semaphorin 6B, which relate to chronic axonal growth arrest and therefore are promising candidates for lesion-induced axonal growth inhibitors. In addition, we observed that within the subiculum, where the fornix axons originate, neuronal Oct-6 was induced and NG2 was down-regulated, indicating that axotomized neurons as well as glial cells react at the level of gene expression to remote axotomy.
authors.affiliation: Molecular Neurobiology Laboratory, Department of Neurology, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, D-40225 Düsseldorf, Germany.
authors.forename: Patrick
authors.initials: P
authors.lastname: Küry
authors.forename: Daniel
authors.initials: D
authors.lastname: Abankwa
authors.forename: Fabian
authors.initials: F
authors.lastname: Kruse
authors.forename: Regine
authors.initials: R
authors.lastname: Greiner-Petter
authors.forename: Hans Werner
authors.initials: HW
authors.lastname: Müller
mesh_terms: D000818:Animals; D000941:Antigens / Q000235:genetics; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D019771:Axotomy; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D002630:Chemotactic Factors / Q000235:genetics*; D020712:Fornix, Brain / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000235:genetics; D020439:Growth Cones / Q000378:metabolism / Q000473:pathology; D006133:Growth Substances / Q000235:genetics*; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D008562:Membrane Glycoproteins / Q000235:genetics; D009416:Nerve Regeneration / Q000235:genetics / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000235:genetics; D009434:Neural Pathways / Q000293:injuries / Q000378:metabolism* / Q000473:pathology; D020411:Oligonucleotide Array Sequence Analysis; D011509:Proteoglycans / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D002630:Chemotactic Factors; D006133:Growth Substances; D008562:Membrane Glycoproteins; D009419:Nerve Tissue Proteins; D011509:Proteoglycans; D012333:RNA, Messenger; D000099216:Chondroitin Sulfate Proteoglycan 4; C110238:Sema6b protein, rat