IR@PKUHSC  > 北京大学第二临床医学院
学科主题临床医学
Inhibition of pathological retinal neovascularization by semaphorin 3A
Yu, Wenzhen1; Bai, Yujing1; Han, Na2; Wang, Fei1; Zhao, Min1; Huang, Lvzhen1; Li, Xiaoxin1
刊名MOLECULAR VISION
2013-06-27
19页:1397-1405
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Ophthalmology
研究领域[WOS]Biochemistry & Molecular Biology ; Ophthalmology
关键词[WOS]ENDOTHELIAL GROWTH-FACTOR ; TUMOR ANGIOGENESIS ; GUIDANCE ; CELLS ; RETINOPATHY ; DISEASE ; CANCER ; MOVE
英文摘要

Objective: Pathological retinal angiogenesis is a major cause of vision loss. Semaphorin 3A (Sema3A), a chemorepellent guidance protein, plays crucial roles in neural and vascular patterning. To identify its role in retinal neovascularization, we investigated its antiangiogenic effects.

Methods: Human umbilical vein endothelial cells (HUVECs) were used for the in vitro study, and an oxygen-induced retinopathy (OIR) mouse model was used for the in vivo study. The HUVECs were incubated with Sema3A, and cell proliferation, migration, apoptosis, cell cycle, tube formation, and c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (p38 MAPK) signaling pathways were measured using Cell Counting Kit-8, Transwell, flow cytometry, Matrigel assays, and western blot. C57BL/6J mouse pups were exposed to 75% oxygen for 5 days and then brought to room air and injected with Sema3A intravitreously. At postnatal day 18, the retinal nonperfused areas were measured. The in vitro and in vivo vascular endothelial growth factor-165 (VEGF(165)) secretion was measured using enzyme-linked immunosorbent assay.

Results: Sema3A not only inhibited VEGF(165)-induced proliferation, but also induced cell cycle arrest in a dose-dependent manner. Furthermore, Sema3A inhibited migration and tube formation, both in general and in VEGF(165)-containing culture medium. Using an enzyme-linked immunosorbent assay, we showed that Sema3A did not affect VEGF(165) secretion, but it did impede VEGF(165) function. Additionally, Sema3A significantly inhibited the phosphorylation of the JNK and p38MAPK signaling pathways. When administered intravitreously, Sema3A reduced the pathological vascular changes seen in the retinal neovascularization OIR model.

Conclusions: These results suggest that the administration of Sema3A could be a useful therapeutic strategy for preventing hypoxia/ischemic-induced retinal neovascularization.

语种英语
WOS记录号WOS:000321205400002
项目编号2011CB510200 ; RDB2012-24
资助机构National Basic Research Program of China (973 Program) ; Peking University People&prime ; s Hospital Research and Development Fund
引用统计
被引频次:13[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56124
专题北京大学第二临床医学院
北京大学第二临床医学院_眼科
作者单位1.Peking Univ, Peoples Hosp, Minist Educ,Dept Ophthalmol, Key Lab Vis Loss & Restorat, Beijing 100044, Peoples R China
2.Peking Univ, Peoples Hosp, Dept Orthopaed & Trauma, Beijing 100044, Peoples R China
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GB/T 7714
Yu, Wenzhen,Bai, Yujing,Han, Na,et al. Inhibition of pathological retinal neovascularization by semaphorin 3A[J]. MOLECULAR VISION,2013,19:1397-1405.
APA Yu, Wenzhen.,Bai, Yujing.,Han, Na.,Wang, Fei.,Zhao, Min.,...&Li, Xiaoxin.(2013).Inhibition of pathological retinal neovascularization by semaphorin 3A.MOLECULAR VISION,19,1397-1405.
MLA Yu, Wenzhen,et al."Inhibition of pathological retinal neovascularization by semaphorin 3A".MOLECULAR VISION 19(2013):1397-1405.
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