| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Regular Articles |
From the Departments of Pediatrics, Pathology, and Microbiology-Immunology, Dalhousie University, Halifax, Nova Scotia, Canada
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-
or interleukin-1)-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, RANTES, MIP-1) 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--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.
This article has been cited by other articles:
 |
|
 |
|
  A. K. Stannard, R. Khurana, I. M. Evans, V. Sofra, D. I.R. Holmes, and I. Zachary Vascular Endothelial Growth Factor Synergistically Enhances Induction of E-Selectin by Tumor Necrosis Factor-{alpha} Arterioscler. Thromb. Vasc. Biol., March 1, 2007; 27(3): 494 - 502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. E. M. Dirkx, M. G. A. oude Egbrink, J. Wagstaff, and A. W. Griffioen Monocyte/macrophage infiltration in tumors: modulators of angiogenesis J. Leukoc. Biol., December 1, 2006; 80(6): 1183 - 1196. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. I. Zittermann and A. C. Issekutz Endothelial growth factors VEGF and bFGF differentially enhance monocyte and neutrophil recruitment to inflammation J. Leukoc. Biol., August 1, 2006; 80(2): 247 - 257. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. F. Rosenberg Interview with Dr. Andrew Issekutz regarding Pivotal Advance: Endothelial growth factors VEGF and bFGF differentially modulate monocyte and neutrophil recruitment to inflammation J. Leukoc. Biol., August 1, 2006; 80(2): 245 - 246. [Full Text] [PDF]
|
|
|
|
 |
|
 A. E. M. Dirkx, M. G. A. oude Egbrink, K. Castermans, D. W. J. van der Schaft, V. L. J. L. Thijssen, R. P. M. Dings, L. Kwee, K. H. Mayo, J. Wagstaff, J. C. A. B. ter Steege, et al. Anti-angiogenesis therapy can overcome endothelial cell anergy and promote leukocyte-endothelium interactions and infiltration in tumors FASEB J, April 1, 2006; 20(6): 621 - 630. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. I. Zittermann and A. C. Issekutz Basic Fibroblast Growth Factor (bFGF, FGF-2) Potentiates Leukocyte Recruitment to Inflammation by Enhancing Endothelial Adhesion Molecule Expression Am. J. Pathol., March 1, 2006; 168(3): 835 - 846. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. C. Kuenen, G. Giaccone, R. Ruijter, A. Kok, C. Schalkwijk, K. Hoekman, and H. M. Pinedo Dose-Finding Study of the Multitargeted Tyrosine Kinase Inhibitor SU6668 in Patients with Advanced Malignancies Clin. Cancer Res., September 1, 2005; 11(17): 6240 - 6246. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-K. Min, Y.-M. Kim, S. W. Kim, M.-C. Kwon, Y.-Y. Kong, I. K. Hwang, M. H. Won, J. Rho, and Y.-G. Kwon TNF-Related Activation-Induced Cytokine Enhances Leukocyte Adhesiveness: Induction of ICAM-1 and VCAM-1 via TNF Receptor-Associated Factor and Protein Kinase C-Dependent NF-{kappa}B Activation in Endothelial Cells J. Immunol., July 1, 2005; 175(1): 531 - 540. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H. Lee, G. T. Oh, S. Y. Park, J.-H. Choi, J.-G. Park, C. D. Kim, W. S. Lee, B. Y. Rhim, Y. W. Shin, and K. W. Hong Cilostazol Reduces Atherosclerosis by Inhibition of Superoxide and Tumor Necrosis Factor-{alpha} Formation in Low-Density Lipoprotein Receptor-Null Mice Fed High Cholesterol J. Pharmacol. Exp. Ther., May 1, 2005; 313(2): 502 - 509. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. A. Curat, A. Miranville, C. Sengenes, M. Diehl, C. Tonus, R. Busse, and A. Bouloumie From Blood Monocytes to Adipose Tissue-Resident Macrophages: Induction of Diapedesis by Human Mature Adipocytes Diabetes, May 1, 2004; 53(5): 1285 - 1292. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. E. M. Dirkx, M. G. A. oude Egbrink, M. J. E. Kuijpers, S. T. van der Niet, V. V. T. Heijnen, J. C. A. B.-t. Steege, J. Wagstaff, and A. W. Griffioen Tumor Angiogenesis Modulates Leukocyte-Vessel Wall Interactions in Vivo by Reducing Endothelial Adhesion Molecule Expression Cancer Res., May 1, 2003; 63(9): 2322 - 2329. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
