Erk- and akt-dependent neuroprotection by erythropoietin (epo) against glyoxal-ages via modulation of bcl-xl, bax, and bad
文献类型：期刊论文
| 作者 | Shen, Jianfeng1,2,3,4,8; Wu, Yalan3,4; Xu, Jing-Ying1,2,3,4; Zhang, Jingfa1,2,3,4; Sinclair, Stephen H.5; Yanoff, Myron5; Xu, Guoxu7; Li, Weiye1,2,3,4,5,6; Xu, Guo-Tong1,2,3,4 |
| 刊名 | Investigative ophthalmology & visual science
 |
| 出版日期 | 2010 |
| 卷号 | 51期号:1页码:35-46 |
| ISSN号 | 0146-0404 |
| DOI | 10.1167/iovs.09-3544 |
| 通讯作者 | Xu, guo-tong(gtxu@tongji.edu.cn) |
| 英文摘要 | Purpose. to characterize the neuroprotective mechanisms of erythropoietin (epo) against the stress of glyoxal-advanced glycation end products (ages) in retinal neuronal cells. methods. rat retinal organ culture, primary retinal neuron culture, and retinal cell line (r28 cell) culture under glyoxal-ages insult were used as in vitro models. exogenous epo was applied to these models. retinal neuronal cell death was assessed by tunel, ethidium bromide/acridine orange staining, and cell viability assay. r28 cell proliferation was evaluated by brdu incorporation and propidium iodide staining. real-time rt-pcr and western blot analysis were used to detect bcl-xl, bcl-2, bax, bad, and products of extracellular signal regulated kinase (erk) and akt pathways. specific inhibitors and plasmids were used to pinpoint the roles of erk and akt pathways. results. epo protected the retinal cells from glyoxal-age-induced injury in a time-and dose-dependent fashion. the protective function of epo was proved to be antiapoptotic, not pro-cell proliferative. glyoxal upregulated bax expression but suppressed bcl-xl expression and bad phosphorylation. in contrast, epo enhanced bad phosphorylation and bcl-xl expression but downregulated bax. the regulation of these apoptosis-related proteins by epo was through erk and akt pathways. conclusions. these data demonstrate that exogenous epo significantly attenuates the retinal neuronal cell death induced by glyoxal-ages by promoting antiapoptotic and suppressing apoptotic proteins. epo/epo receptor signaling through erk and akt pathways is pivotal in epo neuroprotective mechanisms. (invest ophthalmol vis sci. 2010; 51: 35-46) doi: 10.1167/iovs.09-3544 |
| WOS关键词 | RETINAL GANGLION-CELLS ; GLYCATION END-PRODUCTS ; GLOBAL CEREBRAL-ISCHEMIA ; NF-KAPPA-B ; OXIDATIVE STRESS ; ALZHEIMERS-DISEASE ; INDUCED APOPTOSIS ; PROTEIN FAMILY ; GROWTH-FACTOR ; NITRIC-OXIDE |
| WOS研究方向 | Ophthalmology |
| WOS类目 | Ophthalmology |
| 语种 | 英语 |
| WOS记录号 | WOS:000273264200007 |
| 出版者 | ASSOC RESEARCH VISION OPHTHALMOLOGY INC |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2408457 |
| 专题 | 中国科学院大学 |
| 通讯作者 | Xu, Guo-Tong |
| 作者单位 | 1.Tongji Univ, Tongji Eye Inst, Sch Med, Shanghai 200092, Peoples R China 2.Tongji Univ, Dept Regenerat Med, Sch Med, Shanghai 200092, Peoples R China 3.Shanghai Jiao Tong Univ, Sch Med, Shanghai 200030, Peoples R China 4.Chinese Acad Sci, Inst Hlth Sci, Shanghai Inst Biol Sci, Lab Clin Visual Sci, Shanghai, Peoples R China 5.Drexel Univ, Coll Med, Dept Ophthalmol, Philadelphia, PA 19104 USA 6.Chinese Acad Med Sci, Peking Union Med Coll, Dept Ophthalmol, Beijing 100037, Peoples R China 7.Suzhou Univ, Affiliated Hosp 2, Dept Ophthalmol, Suzhou 215006, Peoples R China 8.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China |
| 推荐引用方式 GB/T 7714 | Shen, Jianfeng,Wu, Yalan,Xu, Jing-Ying,et al. Erk- and akt-dependent neuroprotection by erythropoietin (epo) against glyoxal-ages via modulation of bcl-xl, bax, and bad[J]. Investigative ophthalmology & visual science,2010,51(1):35-46. |
| APA | Shen, Jianfeng.,Wu, Yalan.,Xu, Jing-Ying.,Zhang, Jingfa.,Sinclair, Stephen H..,...&Xu, Guo-Tong.(2010).Erk- and akt-dependent neuroprotection by erythropoietin (epo) against glyoxal-ages via modulation of bcl-xl, bax, and bad.Investigative ophthalmology & visual science,51(1),35-46. |
| MLA | Shen, Jianfeng,et al."Erk- and akt-dependent neuroprotection by erythropoietin (epo) against glyoxal-ages via modulation of bcl-xl, bax, and bad".Investigative ophthalmology & visual science 51.1(2010):35-46. |
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来源：中国科学院大学
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