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

The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.

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·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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Crossref · 10.1161/hc0902.104718

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  1. 10.1161/circ.97.4.381 · DOI
  2. 10.1161/circ.101.3.305 · DOI
  3. 10.1161/circ.102.7.806 · DOI
  4. 10.1161/circ.102.18.2243 · DOI
  5. 10.1161/circ.95.6.1532 · DOI
  6. 10.1161/hyp.25.5.913 · DOI

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Metadata

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
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 (medical) › 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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