hVEGFA-TG Mouse
製品名
hVEGFA-TG Mouse
製品ID
C001395
系統名
C57BL/6JCya-Tg(bRho-VEGFA)/Cya
背景情報
C57BL/6JCya
状況
このマウス系統を論文で使用する場合は、「hVEGFA-TG Mouse（カタログ番号C001395）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
遺伝子名
遺伝子別名
VPF, VEGF, MVCD1
NCBI ID
染色体
Chr 6
MGI ID
さらに
系統詳細
The Vascular Endothelial Growth Factor (VEGF) family is a group of particular endothelial growth factors intimately associated with angiogenesis. These factors promote increased vascular permeability, extracellular matrix degeneration, vascular endothelial cell migration and proliferation, and are capable of stimulating angiogenesis and increasing the permeability of existing vessels. As such, they play a pivotal role in normal vascular development and wound healing. The VEGF family comprises VEGFA, VEGFB, VEGFC, VEGFD, VEGFE, and PLGF[1]. Of these, VEGFA is the most commonly targeted in research related to neovascular ophthalmic diseases due to its crucial role in the proliferation, migration, and formation of endothelial cell microvessels[2]. Overexpression of VEGFA in the eye can result in abnormal vascular growth and leakage, leading to various ophthalmic diseases such as Age-Related Macular Degeneration (AMD), Diabetic Retinopathy (DR), and corneal neovascularization[2-3].
The hVEGFA-TG mouse is a transgenic model generated by Cyagen. In this model, the expression of human VEGFA CDS is driven by the bovine rhodopsin promoter, allowing for specific overexpression of the human VEGFA gene in the retina without affecting the expression of the endogenous VEGFA gene. This model exhibits clear retinal and choroidal vascular lesions while maintaining complete eye structure and can naturally develop diseases. Anti-VEGF drugs such as Aflibercept[4] have been evaluated for efficacy in this mouse model, demonstrating that Aflibercept can target and suppress VEGF expression, thereby alleviating retinal vascular lesions. As such, this model is well-suited for drug evaluation and mechanism research related to neovascular ophthalmic diseases.
参考文献
Hoeben A, Landuyt B, Highley MS, Wildiers H, Van Oosterom AT, De Bruijn EA. Vascular endothelial growth factor and angiogenesis. Pharmacol Rev. 2004 Dec;56(4):549-80.
Apte RS, Chen DS, Ferrara N. VEGF in Signaling and Disease: Beyond Discovery and Development. Cell. 2019 Mar 7;176(6):1248-1264.
Mesquita J, Castro-de-Sousa JP, Vaz-Pereira S, Neves A, Passarinha LA, Tomaz CT. Vascular endothelial growth factors and placenta growth factor in retinal vasculopathies: Current research and future perspectives. Cytokine Growth Factor Rev. 2018 Feb;39:102-115.
Stewart MW, Grippon S, Kirkpatrick P. Aflibercept. Nat Rev Drug Discov. 2012 Mar 30;11(4):269-70.Hartong, D. T., Berson, E. L., & Dryja, T. P. (2006). Retinitis pigmentosa. The Lancet, 368(9549), 1795-1809.
系統作製戦略
Figure 1. Diagram of the gene editing strategy employed in the generation of hVEGFA-TG mice. Utilizing transgenic technology, the “Bovine rhodopsin promoter-Kozak-Human VEGFA CDS-Mouse Prm1 polyA” gene expression construct was successfully integrated into the mouse genome. This approach facilitated the specific overexpression of human VEGFA in the retina of hVEGFA-TG mice.
適用分野
Research on Age-Related Macular Degeneration (AMD);
Research on Diabetic Retinopathy (DR);
Research on corneal neovascular diseases.
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