GLCE regulates PC12 cell neuritogenesis induced by nerve growth factor through activating SMAD/ID3 signalling
文献类型：期刊论文
| 作者 | Li, Jie1,2; Fang, Jianping1; Qin, Yi1; Liao, Wenfeng1; Liu, Hailing1; Zhou, Yifa2; Ding, Kan1
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| 刊名 | BIOCHEMICAL JOURNAL
 |
| 出版日期 | 2014-04-15 |
| 卷号 | 459页码:405-415 |
| 关键词 | differentiation glucuronic acid epimerase (GLCE) heparan sulfate inhibitor of DNA binding/differentiation 3 (ID3) neuritogenesis |
| ISSN号 | 0264-6021 |
| DOI | 10.1042/BJ20131360 |
| 文献子类 | Article |
| 英文摘要 | Neurodevelopment is orchestrated by a series of growth factor-HS (heparan sulfate) interactions which are involved in neuritogenesis. GLCE (glucuronic acid epimerase) is a critical enzyme involved in HS synthesis, which converts GlcA (D-glucuronic acid) into IdoA (L-iduronic acid). However, the function of GLCE in neuritogenesis is largely unknown. In the present study we showed that GLCE depletion caused arrested PC12 cell growth and promoted the cell neuritogenesis and differentiation induced by NGF (nerve growth factor). PC12 cell growth was boosted by overexpression of GLCE, and neuritogenesis was impaired when GLCE depletion was rescued. Interestingly, overexpression of wild-type GLCE with Y168A and Y222A mutations led to enhanced PC12 cell growth and attenuated the neuritogenesis triggered by GLCE silencing. We showed further that GLCE depletion blocked SMAD1/5/8 phosphorylation; however, this signalling could be restored by GLCE or the mutation of its active enzymatic site. In addition, the downstream effector of SMAD1/5/8, ID3 (inhibitor of DNA binding/differentiation 3) was induced by GLCE. ID3 silencing inhibited PC12 cell growth and induced cell neuritogenesis and differentiation. In addition, ectopic expression of ID3 partially rescued the phenotype caused by GLCE silencing. The results of the present study suggest that GLCE plays a key role in PC12 cell growth and neuritogenesis through SMAD/ID3 signalling. |
| WOS关键词 | D-GLUCURONYL C5-EPIMERASE ; L-IDURONIC ACID ; HEPARAN-SULFATE ; BREAST-CANCER ; AXON GUIDANCE ; IN-VITRO ; GENE ; ID3 ; EXPRESSION ; DIFFERENTIATION |
| 资助项目 | National Science Fund for Distinguished Young Scholars[81125025] ; New Drug Creation and Manufacturing Program[2012ZX09301001-003] ; National Natural Science Foundation of China[31230022] ; National Natural Science Foundation of China[81171914] |
| WOS研究方向 | Biochemistry & Molecular Biology |
| 语种 | 英语 |
| WOS记录号 | WOS:000334325400015 |
| 出版者 | PORTLAND PRESS LTD |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/277116]  |
| 专题 | 药理学第三研究室 |
| 通讯作者 | Zhou, Yifa |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Mat Med, Glycochem & Glycobiol Lab, Shanghai 201203, Peoples R China 2.NE Normal Univ, Sch Life Sci, Changchun 130024, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Li, Jie,Fang, Jianping,Qin, Yi,et al. GLCE regulates PC12 cell neuritogenesis induced by nerve growth factor through activating SMAD/ID3 signalling[J]. BIOCHEMICAL JOURNAL,2014,459:405-415. |
| APA | Li, Jie.,Fang, Jianping.,Qin, Yi.,Liao, Wenfeng.,Liu, Hailing.,...&Ding, Kan.(2014).GLCE regulates PC12 cell neuritogenesis induced by nerve growth factor through activating SMAD/ID3 signalling.BIOCHEMICAL JOURNAL,459,405-415. |
| MLA | Li, Jie,et al."GLCE regulates PC12 cell neuritogenesis induced by nerve growth factor through activating SMAD/ID3 signalling".BIOCHEMICAL JOURNAL 459(2014):405-415. |
入库方式： OAI收割
来源：上海药物研究所
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