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学科主题: 临床医学
题名:
Effects of Semaphorin 3A on Retinal Pigment Epithelial Cell Activity
作者: Bai, Yujing1; Yu, Wenzhen1; Han, Na2; Yang, Fei1; Sun, Yaoyao1; Zhang, Lijuan1; Zhao, Min1; Huang, Lvzhen1; Zhou, Aiyi1; Wang, Fei1; Li, Xiaoxin1
关键词: semaphorin 3A ; retinal pigment epithelial (RPE) ; vascular endothelial growth factor (VEGF)
刊名: INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
发表日期: 2013-10-01
DOI: 10.1167/iovs.13-12625
卷: 54, 期:10, 页:6628-6637
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Ophthalmology
研究领域[WOS]: Ophthalmology
关键词[WOS]: ENDOTHELIAL GROWTH-FACTOR ; PROLIFERATIVE VITREORETINOPATHY ; DIFFERENTIAL EXPRESSION ; MACULAR DEGENERATION ; UP-REGULATION ; NEUROPILIN-1 ; VEGF ; GUIDANCE ; NEOVASCULARIZATION ; ANGIOGENESIS
英文摘要:

PURPOSE. Semaphorin 3A (Sema3A), a chemorepellant guidance protein, has been shown to be crucial for neural and vascular remodeling. This study is designed to examine the effects of Sema3A on RPE cell activity both in vitro and in vivo.

METHODS. Retinal pigment epithelial were incubated with Sema3A, or VEGF- and Sema3A-containing medium. Cell proliferation, migration, cell cycle, apoptosis, cocultured human umbilical vein endothelial cells tube formation, VEGF receptor 2 (VEGFR2) and neuropilin 1 (Nrp1) receptor expression, VEGF-and pigment epithelium-derived factor (PEDF) concentration, and c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (p38MAPK) signaling pathway studies were measured. A rabbit proliferative vitreoretinopathy (PVR) model was used for in vivo study. Subconfluent ARPE19 cells were injected intravitreously with or without Sema3A. Data were analyzed with Graphpad Prism 5.0 software.

RESULTS. In vitro, Sema3A not only induced RPE cell cycle arrest and inhibited RPE migration under normal culture conditions, but also inhibited exogenous and endogenous VEGF(165)-induced cell activities. These activities included proliferation, migration, cell cycle arrest, JNK and p38MAPK signaling pathway phosphorylation, and cocultured endothelial cell tube formation. It is shown that both VEGF(165) and Sema3A induced the upregulation of VEGFR2 and Nrp1 receptors. Activity inhibition was mediated by impeding VEGF(165) utilization and possibly mediated by competitive inhibition of VEGF(165) binding to its receptor VEGFR2, but not by the suppression of VEGF(165) secretion. In vivo, Sema3A inhibited PVR, which is induced by RPE proliferation.

CONCLUSIONS. These results suggested that Sema3A could be a useful therapeutic strategy for preventing RPE malfunction.

语种: 英语
所属项目编号: RDB2012-24 ; 2011CB510200 ; 81200690
项目资助者: Peking University People&prime ; s Hospital Research and Development Fund ; National Basic Research Program of China (973 Program) ; National Natural Science Foundation of China
WOS记录号: WOS:000326567700021
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/53779
Appears in Collections:北京大学第二临床医学院_眼科_期刊论文

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作者单位: 1.Peking Univ Peoples Hosp, Dept Ophthalmol, Minist Educ, Key Lab Vis Loss & Restorat, Beijing 100044, Peoples R China
2.Peking Univ Peoples Hosp, Dept Orthoped & Trauma, Beijing 100044, Peoples R China

Recommended Citation:
Bai, Yujing,Yu, Wenzhen,Han, Na,et al. Effects of Semaphorin 3A on Retinal Pigment Epithelial Cell Activity[J]. INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE,2013,54(10):6628-6637.
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