Biological Determinants of and Reference Values for Plasma Interleukin-8, Monocyte Chemoattractant Protein-1, Epidermal Growth Factor, and Vascular Endothelial Growth Factor: Results From the STANISLAS Cohort

2007 ◽  
Vol 2007 ◽  
pp. 369-370
Author(s):  
M.G. Bissell
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Vascular Endothelial ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Biological Determinants ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

scholarly journals Biological Determinants of and Reference Values for Plasma Interleukin-8, Monocyte Chemoattractant Protein-1, Epidermal Growth Factor, and Vascular Endothelial Growth Factor: Results from the STANISLAS Cohort

2006 ◽  
Vol 52 (3) ◽  
pp. 504-510 ◽  
Author(s):  
Hind Berrahmoune ◽  
John V Lamont ◽  
Bernard Herbeth ◽  
Peter S FitzGerald ◽  
Sophie Visvikis-Siest
Keyword(s):  
Platelet Count ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Monocyte Count ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Epidermal Growth ◽  
Age Range ◽  
Endothelial Growth Factor

Abstract Background: Interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF) are known to be involved in various diseases related to inflammation, vascular remodeling, or growth deregulation. In addition, increases in plasma concentrations of these cytokines appear to provide useful diagnostic and prognostic information. We therefore investigated which factors most strongly influence the biological variations of plasma IL-8, MCP-1, EGF, and VEGF concentrations. Methods: We used the Evidence® biochip array analyzer to quantify plasma IL-8, MCP-1, EGF, and VEGF concentrations in a subsample of 304 children (age range, 4–17 years) and 540 adults (age range, 18–55 years) from the STANISLAS family study. We also calculated reference intervals for the 4 cytokines. Results: We found the following associations with plasma marker concentrations: Age, neutrophil count, and glucose concentration were positively associated with IL-8 concentrations in children and adults, as were smoking and platelet count in adults. MCP-1 concentrations were associated with age and smoking in both children and adults, monocyte count in children, and sex and hematocrit in adults. EGF concentrations were associated with platelet count in children and monocyte count and glucose in adults. VEGF concentrations were associated with age in children and adults and platelet count and alanine aminotransferase activity in adults. Conclusion: Our results for IL-8, MCP-1, EGF, and VEGF may be useful for interpretation of patients’ laboratory results and for understanding the regulation of concentrations of these cytokines in physiologic conditions.

Monocyte chemoattractant protein-1–induced angiogenesis is mediated by vascular endothelial growth factor-A

Blood ◽  
2005 ◽  
Vol 105 (4) ◽  
pp. 1405-1407 ◽  
Author(s):  
Kyung Hee Hong ◽  
Jewon Ryu ◽  
Ki Hoon Han
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Mitogen Activated Protein Kinase ◽  
Vascular Endothelial ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Endothelial Growth Factor

Abstract Monocyte chemoattractant protein-1 (MCP-1) has been recognized as an angiogenic chemokine. In the present study, we investigated the detailed mechanism by which MCP-1 induces angiogenesis. We found that MCP-1 up-regulated hypoxia-inducible factor 1α (HIF-1α) gene expression in human aortic endothelial cells (HAECs), which induced vascular endothelial growth factor-A165 (VEGF-A165) expression in the aortic wall and HAECs through activation of p42/44 mitogen-activated protein kinase (MAPK). In vivo angiogenesis assay using chick chorioallantoic membrane (CAM) showed that MCP-1–induced angiogenesis was as potent as that induced by VEGF-A165 and completely inhibited by a VEGF inhibitor, Flt2-11. The inhibition of RhoA small G protein did not affect MCP-1–induced VEGF-A165 production and secretion but completely blocked both MCP-1– and VEGF-A–induced new vessel formation, as determined by CAM assay. These results suggest that MCP-1–induced angiogenesis is composed largely of 2 sequential steps: the induction of VEGF-A gene expression by MCP-1 and the subsequent VEGF-A–induced angiogenesis.

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