通过中和抗SDF-1α抗体抑制实验性角膜新生血管形成。
Inhibited experimental corneal neovascularization by neutralizing anti-SDF-1α antibody.
作者信息
Liu Gao-Qin, Lu Pei-Rong, Li Long-Biao, Zhang Xue-Guang
机构信息
Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.
出版信息
Int J Ophthalmol. 2012;5(1):7-12. doi: 10.3980/j.issn.2222-3959.2012.01.02. Epub 2012 Feb 18.
AIM
To explore the effect of SDF-1α on the development of experimental corneal neovascularization (CRNV).
METHODS
CRNV was induced by alkali injury in mice. The expression of SDF-1α and CXCR4 in burned corneas was examined by Flow Cytometry. Neutralizing anti-mouse SDF-1α antibody was locally administrated after alkali injury and the formation of CRNV 2 weeks after injury was assessed by Immunohistochemistry. The expression of VEGF and C-Kit in burned corneas was detected by RT-PCR.
RESULTS
The number of CRNV peaks at 2 weeks after alkali injury. Compared to control group, SDF-1α neutralizing antibody treatment significantly decreased the number of CRNV. RT-PCR confirmed that SDF-1α neutralizing antibody treatment resulted in decreased intracorneal VEGF and C-Kit expression.
CONCLUSION
SDF-1α neutralizing antibody treated mice exhibited impaired experimental CRNV through down regulated VEGF and C-Kit expression.
目的
探讨基质细胞衍生因子-1α（SDF-1α）对实验性角膜新生血管化（CRNV）发展的影响。
方法
通过碱损伤诱导小鼠发生CRNV。采用流式细胞术检测烧伤角膜中SDF-1α和CXC趋化因子受体4（CXCR4）的表达。碱损伤后局部给予抗小鼠SDF-1α中和抗体，并通过免疫组织化学评估损伤后2周CRNV的形成情况。采用逆转录聚合酶链反应（RT-PCR）检测烧伤角膜中血管内皮生长因子（VEGF）和干细胞生长因子受体（C-Kit）的表达。
结果
碱损伤后2周CRNV数量达到峰值。与对照组相比，SDF-1α中和抗体治疗显著减少了CRNV的数量。RT-PCR证实，SDF-1α中和抗体治疗导致角膜内VEGF和C-Kit表达降低。
结论
SDF-1α中和抗体处理的小鼠通过下调VEGF和C-Kit表达，使实验性CRNV受损。
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