Gene transfers of vascular endothelial growth factor-A, vascular endothelial growth factor-B, vascular endothelial growth factor-C, and vascular endothelial growth factor-D have no effects on atherosclerosis in hypercholesterolemic low-density lipoprotein-receptor/apolipoprotein B48-deficient mice
- 1Department of Molecular Medicine, A.I. Virtanen Institute, University of Kuopio, Finland.
- 0Department of Molecular Medicine, A.I. Virtanen Institute, University of Kuopio, Finland.
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View abstract on PubMed
Summary
This summary is machine-generated.Vascular endothelial growth factors (VEGFs) do not promote atherosclerosis in mice. Adenovirus-mediated gene transfer of VEGF-A, -B, -C, or -D showed no proatherogenic effects in hypercholesterolemic mice.
Area Of Science
- Cardiovascular Biology
- Molecular Medicine
- Atherosclerosis Research
Background
- Vascular Endothelial Growth Factors (VEGFs) have proposed roles in large artery health, with potential vasculoprotective or proatherogenic effects.
- Understanding VEGFs' impact is crucial as they are used in human therapies.
- This study investigates the atherogenic potential of VEGF family members.
Purpose Of The Study
- To determine if VEGF-A, -B, -C, or -D enhance atherosclerosis.
- To assess the effects of systemic VEGF gene transfer on lesion development in a mouse model.
Main Methods
- Utilized LDL-receptor/apolipoprotein B48 double-knockout (LDLR/apoB48) mice, a model for human hypercholesterolemia and atherosclerosis.
- Administered systemic adenoviral gene transfer of VEGF-A, -B, -C, -D, or LacZ, alongside rhVEGF-A protein administration.
- Analyzed aortas for atherosclerotic lesions, neovascularization, and cellular composition after 3 months on a Western-type diet.
Main Results
- No statistically significant differences were observed in atherosclerotic lesion size or neovascularization across groups treated with VEGFs or placebo.
- Plasma cholesterol and triglyceride levels remained consistent across all experimental groups.
- Gene transfer of VEGF family members did not alter the cellular composition of aortic lesions.
Conclusions
- Adenovirus-mediated gene transfer of VEGF-A, -B, -C, or -D does not promote atherosclerosis in LDLR/apoB48-deficient mice.
- These findings suggest a lack of proatherogenic effects of these VEGFs in a relevant preclinical model.
- The study provides evidence against a proatherogenic role for these VEGFs in the context of hyperlipidemia.
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