title: Expression of Nogo receptor 1 in microglia during development and following traumatic brain injury.
abstract: As the receptor of myelin associated inhibitory factors Nogo receptor 1 (NgR1) plays an important role in central nervous system (CNS) injury and regeneration. It is found that NgR1 complex acts in neurons to transduce the signals intracelluarly including induction of growth cone collapse, inhibition of axonal regeneration and regulation of nerve inflammation. In recent studies, NgR1 has also been found to be expressed in the microglia. However, NgR1 expressed in microglia in the developing nervous systems and following CNS injury have not been widely investigated. In this study, we detected the expression and cellular localization of NgR1 in microglia during development and following traumatic brain injury (TBI) in mice. The results showed that NgR1 was mainly expressed in microglia during embryonic and postnatal periods. The expression levels peaked at P4 and decreased thereafter into adulthood, while increased significantly with aging representatively at 17 mo. On the other hand, there was no significant difference in the number of double positive NgR1(+)Iba1(+) cells between normal and TBI group. In summary, we first detected the expression of NgR1 in microglia during development and found that NgR1 protein expression increased significantly in microglia with aging. These findings will contribute to make a foundation for subsequent study about the role of NgR1 expressed in microglia on the CNS disorders.
authors.affiliation: Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
authors.forename: Gaoxiang
authors.initials: G
authors.lastname: Liu
authors.affiliation: Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Ni
authors.affiliation: Department of Neurosurgery, Jinling Hospital, Nanjing 210000, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Mao
authors.affiliation: Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
authors.forename: Ming
authors.initials: M
authors.lastname: Yan
authors.affiliation: Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Pang
authors.affiliation: Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China. Electronic address: hliao@cpu.edu.cn.
authors.forename: Hong
authors.initials: H
authors.lastname: Liao
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000166:cytology / Q000196:embryology / Q000254:growth & development; D001930:Brain Injuries / Q000473:pathology*; D002135:Calcium-Binding Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D004622:Embryo, Mammalian; D007839:Functional Laterality; D058851:GPI-Linked Proteins / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008840:Microfilament Proteins / Q000378:metabolism; D017628:Microglia / Q000378:metabolism*; D009185:Myelin Proteins / Q000235:genetics / Q000378:metabolism*; D000070816:Nogo Receptor 1; D012333:RNA, Messenger / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism*; D017475:Receptors, Nerve Growth Factor / Q000235:genetics / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics / Q000378:metabolism
chemical_list: C491049:Aif1 protein, mouse; D002135:Calcium-Binding Proteins; D058851:GPI-Linked Proteins; D008840:Microfilament Proteins; D009185:Myelin Proteins; D000070816:Nogo Receptor 1; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D017475:Receptors, Nerve Growth Factor; D018124:Receptors, Tumor Necrosis Factor; C419790:Rtn4r protein, mouse; C517634:Ngfr protein, mouse; C409471:Tnfrsf19 protein, mouse
keywords: Development; Expression; Microglia; NgR1; Traumatic brain injury