hVEGFA-TG Mouse
Product Name
hVEGFA-TG Mouse
Product ID
C001395
Strain Name
C57BL/6JCya-Tg(bRho-VEGFA)/Cya
Backgroud
C57BL/6JCya
Status
When using this mouse strain in a publication, please cite “hVEGFA-TG Mouse (Catalog C001395) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Gene Name
VEGFA
Gene Alias
VPF, VEGF, MVCD1
NCBI ID
Chromosome
Chr 6 (Human)
MGI ID
Datasheet
Strain Description
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.
Reference
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.
Strain Strategy
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.
Application Area
Research on Age-Related Macular Degeneration (AMD);
Research on Diabetic Retinopathy (DR);
Research on corneal neovascular diseases.
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