title: Nogo-A is involved in secondary axonal degeneration of thalamus in hypertensive rats with focal cortical infarction.
abstract: We investigate whether Nogo-A is involved in the secondary axonal degeneration in the thalamus after distal middle cerebral artery occlusion (MCAO) in stroke-prone renovascular hypertensive rats (RHRSP). The expression of Nogo-A in ipsilateral ventroposterior nucleus (VPN) of the thalamus in RHRSP was observed at 1, 2 and 4 weeks after distal MCAO. In addition, intracerebroventricular infusion of NEP1-40, a Nogo-66 receptor (NgR) antagonist peptide, was administered starting 24 h after MCAO and continued for 1, 2 and 4 weeks, respectively. Axonal damage and regeneration were evaluated by analysis of the immunoreactivity (IR) of amyloid betaA4 precursor protein (APP), growth associated protein 43 (GAP-43) and microtubule associated protein 2 (MAP-2) in ipsilateral VPN of the thalamus at 1, 2 and 4 weeks after distal MCAO. Following ischemia, the expression of Nogo-A in oligodendrocytes increased persistently and its localization became redistributed around damaged axons and dendrites. Administration of NEP1-40 downregulated the expression of Nogo-A, reduced axonal injury and enhanced axonal regeneration. Our data suggest that Nogo-A is involved in secondary axonal degeneration and that inhibition of Nogo-A can reduce neuronal damage in the thalamus after distal MCAO.
authors: Department of Neurology and Stroke Center, The First Affiliated Hospital, Sun Yat-Sen University, No. 58 Zhongshan Road 2, Guangzhou 510080, China.
authors: Fang
authors: F
authors: Wang
authors: Zhijian
authors: Z
authors: Liang
authors: Qinghua
authors: Q
authors: Hou
authors: Shihui
authors: S
authors: Xing
authors: Li
authors: L
authors: Ling
authors: Meixia
authors: M
authors: He
authors: Zhong
authors: Z
authors: Pei
authors: Jinsheng
authors: J
authors: Zeng
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D002544:Cerebral Infarction / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D007150:Immunohistochemistry; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009185:Myelin Proteins / Q000378:metabolism* / Q000494:pharmacology / Q000627:therapeutic use; D009414:Nerve Growth Factors / Q000494:pharmacology / Q000627:therapeutic use; D009416:Nerve Regeneration / Q000187:drug effects / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D000070798:Nogo Proteins; D009836:Oligodendroglia / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D012183:Retrograde Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013788:Thalamus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology; D020651:Ventral Thalamic Nuclei / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D014855:Wallerian Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D009185:Myelin Proteins; C509624:NEP1-40 protein, human; D009414:Nerve Growth Factors; D009419:Nerve Tissue Proteins; D000070798:Nogo Proteins; D010446:Peptide Fragments; C000603199:RTN4 protein, human; C000603197:Rtn4 protein, rat