title: PirB restricts neuronal regeneration in developing rat brain following             hypoxia-ischemia.
abstract: The inhibitors of axonal regeneration in the myelin sheath are considered             to be major contributors to the lack of regeneration in the central nervous system             (CNS) following hypoxic-ischemic (HI) brain damage. As well as the Nogo receptor             (NgR), the paired-immunoglobulin-like receptor B (PirB) is a functional receptor             for the myelin inhibitors of axonal regeneration. The inhibition of PirB and NgR             activities may block most of the inhibitory effects of myelin inhibitors on nerve             regeneration. We observed the PirB protein and mRNA expression in HI-damaged rat             cortical neurons using immunohistochemistry and reverse transcription-polymerase             chain reaction assays. In addition, we treated the HI-damaged rat cortical neurons             using PirB antibodies to observe the regeneration of injured neurons. Moreover,             the Rock II activity in HI-damaged rat cortical neurons treated with PirB antibodies             was observed using western blot analysis. The mRNA and protein levels of PirB             increased in newborn rat cortical neurons following HI damage. Treatment with             PirB antibodies is able to improve axonal regeneration following HI damage compared             with normal axonal growth. Rock II activity also increased in the HI-damaged rat             brain. The inhibition of PirB is therefore a potential therapeutic method to promote             the regeneration of HI-damaged axons and the inhibitory signal may be transduced             through the Rho-ROCK signaling pathway.
authors.affiliation: Department of Pediatrics, West China Second University Hospital, Sichuan University, Sichuan, Chengdu 610041, PR China.
authors.forename: Hua
authors.initials: H
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Xiong
authors.forename: Dezhi
authors.initials: D
authors.lastname: Mu
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015153:Blotting, Western; D001921:Brain / Q000166:cytology; D002478:Cells, Cultured; D004789:Enzyme Activation; D058851:GPI-Linked Proteins / Q000235:genetics / Q000378:metabolism; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D009185:Myelin Proteins / Q000235:genetics / Q000378:metabolism; D009416:Nerve Regeneration; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D000070816:Nogo Receptor 1; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D011971:Receptors, Immunologic / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D054460:rho-Associated Kinases / Q000378:metabolism
chemical_list: D058851:GPI-Linked Proteins; D009185:Myelin Proteins; D000070816:Nogo Receptor 1; C491380:Pirb protein, rat; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; C486581:Rtn4r protein, rat; D054460:rho-Associated Kinases