A novel mechanism underlying the susceptibility of neuronal cells to nitric oxide: the occurrence and regulation of protein s-nitrosylation is the checkpoint
文献类型：期刊论文
| 作者 | He, J.; Wang, T.; Wang, P.; Han, P.; Yin, Q.; Chen, C. |
| 刊名 | Journal of neurochemistry
 |
| 出版日期 | 2007-09-01 |
| 卷号 | 102期号:6页码:1863-1874 |
| 关键词 | Glutathione Neurotoxicity Nitric oxide S-nitrosoglutathione S-nitrosoglutathione reductase (gsnor) S-nitrosation S-nitrosylation |
| ISSN号 | 0022-3042 |
| DOI | 10.1111/j.1471-4159.2007.04651.x |
| 通讯作者 | Chen, c.(changchen@moon.ibp.ac.cn) |
| 英文摘要 | The susceptibility of neuronal cells to nitric oxide (no) is a key issue in no-mediated neurotoxicity. however, the underlying mechanism remains unclear. as a cyclic guanosine monophosphate (cgmp)-independent no signaling pathway, s-nitrosylation (or s-nitrosation) has been suggested to occur as a post-translational modification in parallel with o-phosphorylation. the underlying mechanism of the involvement of protein s-nitrosylation in the susceptibility of neuronal cells to no has been little investigated. in this study, we focused on the role of s-nitrosothiols (rsno) in the susceptibility of a cerebellar cell line r2 to no. our results showed the following: (i) s-nitrosoglutathione (gsno) induced a burst of rsno in gsh-depleted r2 cells, the majority of which were primarily contributed by the s-nitrosylation of proteins (pro-snos), and was followed by severe neuronal necrosis; (ii) the elevation in the level of pro-snos resulted from a dysfunction of s-nitroglutathione reductase (gsnor) as a result of its substrate, gsno, being unavailable in gsh-depleted cells. in the meantime, the suppression of gsnor increased no-mediated neurotoxicity in r2 cells, as well as in cerebellar granule neurons; (iii) our results also demonstrate that the burst of rsno is the "checkpoint" of cell fate: if rsno can be reduced to free thiol proteins, cells will survive; if they are further oxidized, cells will die; and (iv) gsh-ethyl ester and vitamin c protected r2 cells against gsno neurotoxicity through two distinct mechanisms: by inhibiting the elevation of pro-snos and by reducing pro-snos to free thiol proteins, respectively. a novel mechanism underlying the susceptibility of neuronal cells to no is proposed and some potential strategies to prevent the no-mediated neurotoxicity are discussed. |
| WOS关键词 | OXIDATIVE STRESS ; PARKINSONS-DISEASE ; FOCAL ISCHEMIA ; CLASS-III ; GLUTATHIONE ; SYNTHASE ; RECEPTOR ; BRAIN ; NITROSOGLUTATHIONE ; DEHYDROGENASE |
| WOS研究方向 | Biochemistry & Molecular Biology ; Neurosciences & Neurology |
| WOS类目 | Biochemistry & Molecular Biology ; Neurosciences |
| 语种 | 英语 |
| WOS记录号 | WOS:000249452000014 |
| 出版者 | BLACKWELL PUBLISHING |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2383515 |
| 专题 | 中国科学院大学 |
| 通讯作者 | Chen, C. |
| 作者单位 | 1.Chinese Acad Sci, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China 2.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China |
| 推荐引用方式 GB/T 7714 | He, J.,Wang, T.,Wang, P.,et al. A novel mechanism underlying the susceptibility of neuronal cells to nitric oxide: the occurrence and regulation of protein s-nitrosylation is the checkpoint[J]. Journal of neurochemistry,2007,102(6):1863-1874. |
| APA | He, J.,Wang, T.,Wang, P.,Han, P.,Yin, Q.,&Chen, C..(2007).A novel mechanism underlying the susceptibility of neuronal cells to nitric oxide: the occurrence and regulation of protein s-nitrosylation is the checkpoint.Journal of neurochemistry,102(6),1863-1874. |
| MLA | He, J.,et al."A novel mechanism underlying the susceptibility of neuronal cells to nitric oxide: the occurrence and regulation of protein s-nitrosylation is the checkpoint".Journal of neurochemistry 102.6(2007):1863-1874. |
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来源：中国科学院大学
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