Curcumin inhibits angiogenesis by up-regulation of microRNA-1275 and microRNA-1246: a promising therapy for treatment of corneal neovascularization

Objective Curcumin (capable of inhibiting angiogenic growth of human umbilical vein endothelial cells [HUVECs]), can be employed in vitro as a model of pathogenesis of corneal neovascularization (CRNV). The aim of this study was to explore regulatory mechanisms of microRNA (miR) levels after curcumi...

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Veröffentlicht in:Cell proliferation 2016-12, Vol.49 (6), p.751-762
Hauptverfasser: Bai, Yanhui, Wang, Weiqun, Sun, Guangli, Zhang, Mingchang, Dong, Jingmin
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Sprache:eng
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Zusammenfassung:Objective Curcumin (capable of inhibiting angiogenic growth of human umbilical vein endothelial cells [HUVECs]), can be employed in vitro as a model of pathogenesis of corneal neovascularization (CRNV). The aim of this study was to explore regulatory mechanisms of microRNA (miR) levels after curcumin treatment. Materials and methods Expression profiles of miRs in curcumin‐treated HUVECs were investigated by miR microassay. Specific mimics and inhibitors of miR‐1275 or miR‐1246 were transfected into HUVECs. Then, their target genes, vascular endothelial growth factor B (VEGFB) and nuclear transcription factor kappa B acting protein (NKAP) were detected by quantitative real‐time PCR, Western blotting assay or immunofluorescence assay. Cell proliferation and cell cycle parameters were measured with the help of CCK‐8 assay and flow cytometry. Results MiR‐1275 and miR‐1246 expression levels were up‐regulated by curcumin. Administration of the specific mimics and inhibitors of the two miRs led to significant changes in expression of VEGFB and NKAP as well as the indicators related to angiogenesis. Anti‐angiogenic effect of curcumin depended on expression patterns of the two miRs in that inhibition of either miR interfered with the effect of curcumin. Furthermore, overexpression of NKAP interrupted effects of curcumin on the cells. Conclusion Collectively, our findings demonstrate that curcumin inhibited HUVEC proliferation by up‐regulation of miR‐1275 and miR‐1246.
ISSN:0960-7722
1365-2184
DOI:10.1111/cpr.12289