ArticleExperimental and therapeutic medicine2019
Antagonistic effects of exogenous Slit2 on VEGF-induced choroidal endothelial cell migration and tube formation.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- The Inhibitory Effects of Gold Nanoparticles on VEGF-A-Induced Cell Migration in Choroid-Retina Endothelial Cells.International journal of molecular sciences · 2019Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial growth factor (VEGF) is involved in the pathogenesis of choroidal neovascularization. The aim of the present study was to assess the effects of exogenous slit guidance ligand 2 (Slit2) on VEGF-induced choroidal endothelial cell (CEC) migration and tube formation. The protein and mRNA expression levels of Slit2, roundabout guidance receptor (Robo) 1 and Robo4 in CECs were evaluated by immunocytochemistry and reverse transcription-polymerase chain reaction analyses, respectively. Western blot analysis was used to assess Robo4 protein levels in CECs exposed to increasing concentrations (0, 50, 75, 100, 125 and 150 ng/ml) of exogenous Slit2. The effects of exogenous Slit2 (125 ng/ml) on VEGF-induced CEC migration and tube formation were also examined. CECs expressed Slit2 and Robo4, but lacked Robo1 expression, at the mRNA and protein levels. Robo4 protein expression increased significantly following treatment with 50-150 ng/ml exogenous Slit2. No significant difference in Robo4 protein expression was observed in CECs treated with 125 and 150 ng/ml Slit2. VEGF-induced CEC migration and tube formation were significantly reduced following treatment with 125 ng/ml exogenous Slit2. In conclusion, these results indicate that Robo4 is expressed in CECs. In addition, exogenous Slit2 may regulate Robo4 expression and partially inhibit VEGF-induced CEC migration and tube formation.
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