論文 - 詳細
| RRC ID | 77846 |
|---|---|
| 著者 | Satoh JI, Kuroda Y. |
| タイトル | Cytokines and neurotrophic factors fail to affect Nogo-A mRNA expression in differentiated human neurones: implications for inflammation-related axonal regeneration in the central nervous system. |
| ジャーナル | Neuropathol Appl Neurobiol |
| Abstract |
Nogo is a novel myelin-associated inhibitor of neurite outgrowth which regulates stable neuronal connections during axonal regeneration following injury in the adult mammalian central nervous system (CNS). Because cytokines and neurotrophic factors play a key role in inflammation-related axonal regeneration, we investigated: (i) the constitutive expression of Nogo and the Nogo receptor (NgR) mRNA in human neural cell lines; (ii) Nogo and NgR mRNA levels in the NTera2 human teratocarcinoma cell line during retinoic acid (RA)-induced neuronal differentiation; and (iii) their regulation in NTera2-derived differentiated neurones (NTera2-N) after exposure to a battery of cytokines and growth factors potentially produced by activated glial cells at post-traumatic inflammatory lesions in the CNS. By reverse transcriptase-polymerase chain reaction analysis, the constitutive expression of Nogo-A, the longest isoform of three distinct Nogo transcripts and NgR mRNA was identified in a wide variety of human neural and non-neural cell lines. By Northern blot analysis, the levels of Nogo-A mRNA were elevated markedly in NTera2 cells following RA-induced neuronal differentiation, accompanied by an increased expression of the neurite growth-associated protein GAP-43 mRNA. In contrast, Nogo-A, Nogo-B, NgR and GAP-43 mRNA levels were unaltered in NTera2-N cells by exposure to basic fibroblast growth factor, brain-derived neurotrophic factor, glia-derived neurotrophic factor, tumour necrosis factor-alpha, interleukin-1beta, dibutyryl cyclic AMP or phorbol 12-myristate 13-acetate. These results indicate that both Nogo-A and NgR mRNA are coexpressed in various human cell types, including differentiated neurones, where their expression is unaffected by exposure to a panel of cytokines and neurotrophic factors which might be involved in inflammation-related axonal regeneration in the CNS. |
| 巻・号 | 28(2) |
| ページ | 95-106 |
| 公開日 | 2002-4-1 |
| DOI | 10.1046/j.1365-2990.2002.00375.x |
| PII | 375 |
| PMID | 11972796 |
| MeSH | Axons / physiology Cell Differentiation / physiology Central Nervous System Diseases / physiopathology Cytokines / pharmacology* GAP-43 Protein / genetics GPI-Linked Proteins Humans Inflammation / physiopathology Myelin Proteins / metabolism* Nerve Growth Factors / pharmacology* Nerve Regeneration / physiology Neurons / cytology* Neurons / metabolism* Nogo Proteins Nogo Receptor 1 RNA, Messenger / metabolism* Receptors, Cell Surface / metabolism Tumor Cells, Cultured Up-Regulation / drug effects |
| IF | 7.5 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
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| 最多言及媒体 | Patent(IFI CLAIMS) |
| 各媒体での言及数の合計 | 3 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| ヒト・動物細胞 | SK-N-SH(RCB0426) |