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dc.contributor.authorWang, L
dc.contributor.authorLee, AYW
dc.contributor.authorWigg, JP
dc.contributor.authorPeshavariya, H
dc.contributor.authorLiu, P
dc.contributor.authorZhang, H
dc.date.accessioned2020-12-22T04:02:00Z
dc.date.available2020-12-22T04:02:00Z
dc.date.issued2016-06-01
dc.identifierpii: ijms17060895
dc.identifier.citationWang, L., Lee, A. Y. W., Wigg, J. P., Peshavariya, H., Liu, P. & Zhang, H. (2016). miR-126 Regulation of Angiogenesis in Age-Related Macular Degeneration in CNV Mouse Model. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 17 (6), https://doi.org/10.3390/ijms17060895.
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/11343/257981
dc.description.abstractmiR-126 has recently been implicated in modulating angiogenic factors in vascular development. Understandings its biological significance might enable development of therapeutic interventions for diseases like age-related macular degeneration (AMD). We aimed to determine the role of miR-126 in AMD using a laser-induced choroidal neovascularization (CNV) mouse model. CNV was induced by laser photocoagulation in C57BL/6 mice. The CNV mice were transfected with scrambled miR or miR-126 mimic. The expression of miR-126, vascular endothelial growth factor-A (VEGF-A), Kinase insert domain receptor (KDR) and Sprouty-related EVH1 domain-containing protein 1 (SPRED-1) in ocular tissues were analyzed by qPCR and Western blot. The overexpression effects of miR-126 were also proven on human microvascular endothelial cells (HMECs). miR-126 showed a significant decrease in CNV mice (p < 0.05). Both mRNA and protein levels of VEGF-A, KDR and SPRED-1 were upregulated with CNV; these changes were ameliorated by restoration of miR-126 (p < 0.05). CNV was reduced after miR-126 transfection. Transfection of miR-126 reduced the HMECs 2D-capillary-like tube formation (p < 0.01) and migration (p < 0.01). miR-126 has been shown to be a negative modulator of angiogenesis in the eye. All together these results high lights the therapeutic potential of miR-126 suggests that it may contribute as a putative therapeutic target for AMD in humans.
dc.languageEnglish
dc.publisherMDPI
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titlemiR-126 Regulation of Angiogenesis in Age-Related Macular Degeneration in CNV Mouse Model
dc.typeJournal Article
dc.identifier.doi10.3390/ijms17060895
melbourne.affiliation.departmentCentre for Eye Research Australia (CERA)
melbourne.source.titleInternational Journal of Molecular Sciences
melbourne.source.volume17
melbourne.source.issue6
dc.rights.licenseCC BY
melbourne.elementsid1183501
melbourne.contributor.authorZHANG, HONG
melbourne.contributor.authorPeshavariya, Hitesh
dc.identifier.eissn1422-0067
melbourne.accessrightsOpen Access


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