Vascular Endothelial Growth Factor Is Necessary in the Development of Arteriosclerosis by Recruiting/Activating Monocytes in a Rat Model of Long-Term Inhibition of Nitric Oxide Synthesis

Zhao, Qingwei; Egashira, Kensuke; Inoue, Shujiro; Usui, Makoto; Kitamoto, Shiro; Ni, Weihua; Ishibashi, Minako; Hiasa, Ken-ichi; Ichiki, Toshihiro; Shibuya, Masabumi; Takeshita, Akira

doi:10.1161/hc0902.104718

Cited by 136Nitric Oxide and Endothelin EffectsAtherosclerosis and Cardiovascular DiseasesAngiogenesis and VEGF in Cancer

Vascular Endothelial Growth Factor Is Necessary in the Development of Arteriosclerosis by Recruiting/Activating Monocytes in a Rat Model of Long-Term Inhibition of Nitric Oxide Synthesis

Zhao, Qingwei, Egashira, Kensuke, Inoue, Shujiro, Usui, Makoto, Kitamoto, Shiro, Ni, Weihua, Ishibashi, Minako, Hiasa, Ken-ichi +3 more·2002·Circulation

DOI 10.1161/hc0902.104718

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Abstract

Background — It remains unclear whether vascular endothelial growth factor (VEGF) is a proarteriosclerotic or an antiarteriosclerotic factor. We recently reported that long-term inhibition of nitric oxide by administering Nω -nitro- l -arginine methyl ester (L-NAME) induces coronary vascular inflammation and arteriosclerosis. Methods and Results — We used this animal model to investigate the role of VEGF in arteriosclerosis. We blocked VEGF activity in vivo by transfecting with plasmid DNA encoding the murine soluble FLT-1 ( sFLT-1 ) gene into thigh muscle. Soluble FLT-1 can suppress VEGF activity both by sequestering VEGF and by functioning as a dominant-negative inhibitor of VEGF receptors. We observed vascular inflammation associated with increased VEGF expression within 3 days of L-NAME administration, which was prevented by pretreatment with ACE inhibitor, angiotensin II receptor antagonist, or neutralizing monocyte chemoattractant protein-1 antibody. The sFLT-1 gene transfer attenuated the early vascular inflammation and prevented late arteriosclerosis. The sFLT-1 gene transfer also inhibited increased expression of monocyte chemoattractant protein-1 and transforming growth factor-β, indicating creation of a positive feedback loop to cause arteriosclerosis. Conclusions — VEGF is necessary in the development of arteriosclerosis by mediating monocyte recruitment and activation in this model.

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A concern regarding VEGF use is increased local inflammation because cell migration and proliferation also correlate with angiogenesis.
“A concern regarding VEGF use is increased local inflammation because cell migration and proliferation also correlate with angiogenesis.200–201”
From Biocompatible Materials for Continuous Glucose Monitoring Devices (2013) · cites this paper as [200]

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Authors: Zhao, Q., Egashira, K., Inoue, S., Usui, M., Kitamoto, S., Ni, W., Ishibashi, M., Hiasa, K.-I., Ichiki, T., Shibuya, M., & Takeshita, A.
Affiliations: Kyushu University (JP)
ORCID: Zhao, Qingwei
Inoue, Shujiro
Usui, Makoto
Ni, Weihua
Hiasa, Ken-ichi
Shibuya, Masabumi
Takeshita, Akira
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2002-03-05
Volume: 105
Issue: 9
Pages: 1110-1115
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/hc0902.104718
OpenAlex: W2159600810
Cited by: 136
References: 20
Citations by year: 2025: 1 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 4 · 2015: 3 · 2014: 5 · 2013: 4 · 2012: 2
FWCI: 11.39
Type: journal article
Language: en
Open access: closed
Locations: Circulation (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Keywords: vascular endothelial growth factor, arteriosclerosis, nitric oxide inhibition, L-NAME, soluble Flt-1, monocyte recruitment, monocyte activation, vascular inflammation, MCP-1, TGF-beta, ACE inhibitors, angiotensin receptor blockers, gene transfer, coronary arteries
MeSH terms: Animals, Arteriosclerosis, Biological Assay, Blood Pressure, Cell Division, Chemotaxis, Leukocyte, Coronary Vessels, Disease Models, Animal, Enzyme Inhibitors, Genetic Vectors, Inflammation, Injections, Intramuscular, Peptidyl-Dipeptidase A, Lymphokines, Male, Monocytes, Nitric Oxide, Proto-Oncogene Proteins, Rats, Inbred WKY, RNA, Messenger, Time, Gene Expression, Transforming Growth Factor beta, Endothelial Growth Factors, Neovascularization, Physiologic, Chemokine CCL2, NG-Nitroarginine Methyl Ester, Receptor Protein-Tyrosine Kinases, Gene Transfer, Horizontal, Vascular Endothelial Growth Factor Receptor-1, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Mice, Rats

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Vascular Endothelial Growth Factor Is Necessary in the Development of Arteriosclerosis by Recruiting/Activating Monocytes in a Rat Model of Long-Term Inhibition of Nitric Oxide Synthesis

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