Molecular vision · 2012
ADP-ribosylation factor as a novel target for corneal neovascularization regression.
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Dai Chunyan, Liu Gaoqin, Li Longbiao, Xiao Yanhui, Zhang Xueguang, Lu Peirong
Аннотация
PURPOSE: To evaluate the roles of ADP-ribosylation factor (ARF) in alkali-induced corneal neovascularization (CNV).
METHODS: CNV was induced by alkali injury and compared in ARF1 inhibitor- or vehicle-treated mice 3 weeks after injury. Angiogenic and apoptosis factor expression in corneas after injury was quantified with reverse-transcription PCR. Human retinal endothelial cell apoptosis induced by ARF1 inhibitor was detected with flow cytometry.
RESULTS: The mRNA expression of ARF1 was augmented in the corneas after alkali injury. Compared with vehicle-treated mice, ARF1 inhibitor-treated mice exhibited impaired CNV 3 weeks after injury, as evidenced by corneal whole mount CD31-staining. Concomitantly, the enhancement of intraocular vascular endothelial growth factor expression was reduced in ARF1 inhibitor-treated mice compared to control mice after injury. Moreover, local administration of the ARF1 inhibitor after alkali injury enhanced intraocular caspase-3 expression. ARF1 inhibitor treatment can significantly induce human retinal endothelial cell apoptosis.
CONCLUSIONS: The ARF1 inhibitor can induce the regression of alkali-induced CNV through increased endothelial cell apoptosis and downregulated intracorneal VEGF expression. ARF1 is an effective intervention target for CNV.
METHODS: CNV was induced by alkali injury and compared in ARF1 inhibitor- or vehicle-treated mice 3 weeks after injury. Angiogenic and apoptosis factor expression in corneas after injury was quantified with reverse-transcription PCR. Human retinal endothelial cell apoptosis induced by ARF1 inhibitor was detected with flow cytometry.
RESULTS: The mRNA expression of ARF1 was augmented in the corneas after alkali injury. Compared with vehicle-treated mice, ARF1 inhibitor-treated mice exhibited impaired CNV 3 weeks after injury, as evidenced by corneal whole mount CD31-staining. Concomitantly, the enhancement of intraocular vascular endothelial growth factor expression was reduced in ARF1 inhibitor-treated mice compared to control mice after injury. Moreover, local administration of the ARF1 inhibitor after alkali injury enhanced intraocular caspase-3 expression. ARF1 inhibitor treatment can significantly induce human retinal endothelial cell apoptosis.
CONCLUSIONS: The ARF1 inhibitor can induce the regression of alkali-induced CNV through increased endothelial cell apoptosis and downregulated intracorneal VEGF expression. ARF1 is an effective intervention target for CNV.
Предметные рубрики MeSH
ADP-Ribosylation Factor 1AlkaliesAnimalsApoptosisCaspase 3CorneaCorneal NeovascularizationEndothelial CellsEnzyme InhibitorsFlow CytometryGene ExpressionHumansMaleMiceMice, Inbred BALB CPlatelet Endothelial Cell Adhesion Molecule-1RetinaReverse Transcriptase Polymerase Chain ReactionVascular Endothelial Growth Factor A