ArticleThe American journal of pathology2002
Down-modulation of monocyte transendothelial migration and endothelial adhesion molecule expression by fibroblast growth factor: reversal by the anti-angiogenic agent SU6668.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 74 citations in OpenAlex.
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- Cytokine inflammatory response in dairy cows with mastitis caused byJournal of veterinary research · 2024Article
- Modulation of T cell function and survival by the tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- Encapsulation of berberine decorated ZnO nano-colloids into injectable hydrogel using for diabetic wound healing.Frontiers in chemistry · 2022Article
- Endothelial Cell Adhesion Molecules- (un)Attainable Targets for Nanomedicines.Frontiers in medical technology · 2022Review
- Anti-angiogenic agents - overcoming tumour endothelial cell anergy and improving immunotherapy outcomes.Nature reviews. Clinical oncology · 2021Review
- Inflammation-Mediated Angiogenesis in Ischemic Stroke.Frontiers in cellular neuroscience · 2021Review
- Long Pentraxin-3 Modulates the Angiogenic Activity of Fibroblast Growth Factor-2.Frontiers in immunology · 2018Review
- Fine-Tuning Tumor Endothelial Cells to Selectively Kill Cancer.International journal of molecular sciences · 2017Review
- Fibroblast growth factors, old kids on the new block.Seminars in cell & developmental biology · 2016Review
- Effective treatment of steatosis and steatohepatitis by fibroblast growth factor 1 in mouse models of nonalcoholic fatty liver disease.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- The Role of the Tumor Vasculature in the Host Immune Response: Implications for Therapeutic Strategies Targeting the Tumor Microenvironment.Frontiers in immunology · 2016Review
- Selenium inhibits LPS-induced pro-inflammatory gene expression by modulating MAPK and NF-κB signaling pathways in mouse mammary epithelial cells in primary culture.Inflammation · 2014Article
- Astragalus polysaccharides suppress ICAM-1 and VCAM-1 expression in TNF-α-treated human vascular endothelial cells by blocking NF-κB activation.Acta pharmacologica Sinica · 2013Article
- Cytokines in pericardial effusion of patients with inflammatory pericardial disease.Mediators of inflammation · 2012Article
- Cathepsin K deficiency reduces elastase perfusion-induced abdominal aortic aneurysms in mice.Arteriosclerosis, thrombosis, and vascular biology · 2012Article
- Phase I, pharmacokinetic, and biological studies of TSU-68, a novel multiple receptor tyrosine kinase inhibitor, administered after meals with solid tumors.Cancer chemotherapy and pharmacology · 2011Article
- Article
- A pro-inflammatory signature mediates FGF2-induced angiogenesis.Journal of cellular and molecular medicine · 2009Article
- Chemokine receptor CXCR4 as a therapeutic target for neuroectodermal tumors.Seminars in cancer biology · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basic and acidic fibroblast growth factor (bFGF and aFGF, respectively) and vascular endothelial growth factor (VEGF) exert angiogenic actions and have a role in wound healing, inflammation, and tumor growth. Monocytes and endothelial cells are involved in these processes, but the effect of FGF and VEGF on monocyte-endothelial cell interactions has not been defined. We observed that monocyte adhesion to resting or cytokine (tumor necrosis factor-alpha or interleukin-1 alpha)-stimulated human umbilical vein endothelial cells (HUVECs) was markedly inhibited (40 to 65%) by culture (1 to 6 days) of HUVECs with aFGF or bFGF. Monocyte transendothelial migration induced by C5a and chemokines (MCP-1, SDF-1 alpha, RANTES, MIP-1 alpha) was also suppressed (by 50 to 75%) on bFGF-stimulated HUVECs. VEGF did not have these effects at the concentrations used (10 to 20 ng/ml), although like bFGF, it promoted HUVEC proliferation. Culture of HUVECs with bFGF and aFGF significantly down-regulated intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin expression on resting or tumor necrosis factor-alpha-stimulated HUVECs, but had no influence on platelet endothelial cell adhesion molecule (PECAM)-1 and VE-cadherin expression. bFGF also inhibited MCP-1 production by HUVECs. The inhibitory effects of bFGF on monocyte transendothelial migration and adhesion molecule expression were reversed by SU6668, an anti-angiogenic agent and bFGF receptor tyrosine kinase inhibitor. Our results suggest that bFGF and aFGF may suppress endothelial-dependent monocyte recruitment and thus have an anti-inflammatory action during angiogenesis in chronic inflammation but inhibit the immunoinflammatory tumor defense mechanism. However, SU6668 is an effective agent to prevent this down-regulatory action of bFGF on monocyte-endothelial cell interactions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.