scholarly journals Membrane Type 1-Matrix Metalloproteinase Is Regulated by Chemokines Monocyte-Chemoattractant Protein-1/CCL2 and Interleukin-8/CXCL8 in Endothelial Cells during Angiogenesis

2004 ◽  
Vol 280 (2) ◽  
pp. 1292-1298 ◽  
Author(s):  
Beatriz G. Gálvez ◽  
Laura Genís ◽  
Salomón Matías-Román ◽  
Samantha A. Oblander ◽  
Karl Tryggvason ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Matrix Metalloproteinase ◽  
Interleukin 8 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Membrane Type

scholarly journals Production of chemokines, interleukin-8 and monocyte chemoattractant protein-1, during monocyte: endothelial cell interactions

Blood ◽  
1995 ◽  
Vol 86 (7) ◽  
pp. 2767-2773 ◽  
Author(s):  
NW Lukacs ◽  
RM Strieter ◽  
V Elner ◽  
HL Evanoff ◽  
MD Burdick ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Interactions ◽  
Interleukin 8 ◽  
Mrna Levels ◽  
Ifn Gamma ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Soluble Collagen

The extravasation of leukocytes from the lumen of the vessel to a site of inflammation requires specific binding events. The interaction of leukocytes with endothelium, via specific receptors, may provide intracellular signals that activate extravasating cells. In the present study, we have investigated the production of chemokines, interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) during monocyte: endothelial cell interactions. Both unstimulated and interferon-gamma (IFN-gamma)-prestimulated human umbilical vein endothelial cells (HUVEC) produced low constitutive levels of IL-8 and MCP-1. The addition of enriched monocytes with unstimulated HUVEC resulted in synergistic increases in production of both IL-8 and MCP-1. Monocytes cultured with IFN-gamma-preactivated HUVECs demonstrated little additional increase in IL-8 and MCP-1 production in coculture assays compared with unstimulated HUVEC. Northern blot analysis paralleled the protein data, demonstrating upregulated expression of IL-8 and MCP-1 mRNA in stimulated and unstimulated coculture assays. Culture of enriched monocytes and endothelial cells in transwells demonstrated no increases in IL-8 or MCP-1, indicating the necessity for cellular contact for chemokine production. In previous investigations, we have demonstrated that increased monocyte-derived MIP-1 alpha production was induced by intracellular adhesion molecule-1 (ICAM-1) interactions on activated HUVECs. In contrast, addition of anti-ICAM-1 monoclonal antibodies (MoAbs) did not diminish the production of IL-8 and MCP-1 in the present study. Furthermore, neither antibodies to IL-1 nor tumor necrosis factor (TNF) diminished the production of either IL-8 or MCP- 1. However, when soluble matrix proteins were added to the coculture to block cellular interactions, the chemokine protein and mRNA levels were significantly decreased. IL-8 production was decreased by both soluble collagen and fibronectin, whereas MCP-1 was decreased by only soluble collagen, suggesting differential activation pathways. These results indicate that IL-8 and MCP-1 production are increased during monocyte and endothelial cell interactions in part due to matrix protein binding mechanisms. This mechanism may serve a role in cell activation, production of chemokines, as well as extravasation and recruitment of additional leukocytes during inflammatory responses.

scholarly journals Reduction of Monocyte Chemoattractant Protein-1 and Interleukin-8 Levels by Ticlopidine in TNF-αStimulated Human Umbilical Vein Endothelial Cells

2009 ◽  
Vol 2009 ◽  
pp. 1-10 ◽  
Author(s):  
Chaur-Jong Hu ◽  
Yueh-Lun Lee ◽  
Neng-Yao Shih ◽  
Yi-Yuan Yang ◽  
Suparat Charoenfuprasert ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Thrombus Formation ◽  
Umbilical Vein ◽  
Interleukin 8 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Human Umbilical Vein ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Treatment And Prevention ◽  
Umbilical Vein Endothelial Cells

Atherosclerosis and its associated complications represent major causes of morbidity and mortality in the industrialized or Western countries. Monocyte chemoattractant protein-1 (MCP-1) is critical for the initiating and developing of atherosclerotic lesions. Interleukin-8 (IL-8), a CXC chemokine, stimulates neutrophil chemotaxis. Ticlopidine is one of the antiplatelet drugs used to prevent thrombus formation relevant to the pathophysiology of atherothrombosis. In this study, we found that ticlopidine dose-dependently decreased the mRNA and protein levels of TNF-α-stimulated MCP-1, IL-8, and vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs). Ticlopidine declined U937 cells adhesion and chemotaxis as compared to TNF-αstimulated alone. Furthermore, the inhibitory effects were neither due to decreased HUVEC viability, nor through NF-kB inhibition. These results suggest that ticlopidine decreased TNF-αinduced MCP-1, IL-8, and VCAM-1 levels in HUVECs, and monocyte adhesion. Therefore, the data provide additional therapeutic machinery of ticlopidine in treatment and prevention of atherosclerosis.

scholarly journals Production of chemokines, interleukin-8 and monocyte chemoattractant protein-1, during monocyte: endothelial cell interactions

Blood ◽  
1995 ◽  
Vol 86 (7) ◽  
pp. 2767-2773 ◽  
Author(s):  
NW Lukacs ◽  
RM Strieter ◽  
V Elner ◽  
HL Evanoff ◽  
MD Burdick ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Interactions ◽  
Interleukin 8 ◽  
Mrna Levels ◽  
Ifn Gamma ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Soluble Collagen

Abstract The extravasation of leukocytes from the lumen of the vessel to a site of inflammation requires specific binding events. The interaction of leukocytes with endothelium, via specific receptors, may provide intracellular signals that activate extravasating cells. In the present study, we have investigated the production of chemokines, interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) during monocyte: endothelial cell interactions. Both unstimulated and interferon-gamma (IFN-gamma)-prestimulated human umbilical vein endothelial cells (HUVEC) produced low constitutive levels of IL-8 and MCP-1. The addition of enriched monocytes with unstimulated HUVEC resulted in synergistic increases in production of both IL-8 and MCP-1. Monocytes cultured with IFN-gamma-preactivated HUVECs demonstrated little additional increase in IL-8 and MCP-1 production in coculture assays compared with unstimulated HUVEC. Northern blot analysis paralleled the protein data, demonstrating upregulated expression of IL-8 and MCP-1 mRNA in stimulated and unstimulated coculture assays. Culture of enriched monocytes and endothelial cells in transwells demonstrated no increases in IL-8 or MCP-1, indicating the necessity for cellular contact for chemokine production. In previous investigations, we have demonstrated that increased monocyte-derived MIP-1 alpha production was induced by intracellular adhesion molecule-1 (ICAM-1) interactions on activated HUVECs. In contrast, addition of anti-ICAM-1 monoclonal antibodies (MoAbs) did not diminish the production of IL-8 and MCP-1 in the present study. Furthermore, neither antibodies to IL-1 nor tumor necrosis factor (TNF) diminished the production of either IL-8 or MCP- 1. However, when soluble matrix proteins were added to the coculture to block cellular interactions, the chemokine protein and mRNA levels were significantly decreased. IL-8 production was decreased by both soluble collagen and fibronectin, whereas MCP-1 was decreased by only soluble collagen, suggesting differential activation pathways. These results indicate that IL-8 and MCP-1 production are increased during monocyte and endothelial cell interactions in part due to matrix protein binding mechanisms. This mechanism may serve a role in cell activation, production of chemokines, as well as extravasation and recruitment of additional leukocytes during inflammatory responses.

scholarly journals Knockdown of Microrna-1260 Promotes Up-Regulation of Both Collagen Type 1 Alpha 1 and Monocyte Chemoattractant Protein-1 in Vascular Smooth Muscle Cells from Human Abdominal Aortic Tissues

2020 ◽  
Vol 7 (1) ◽  
pp. 1103-1103
Author(s):  
Crystal Yin Tung CHAN ◽  
Bernice Lai Yee CHEUK ◽  
Stephen Wing Keung CHENG
Keyword(s):  
Smooth Muscle ◽  
Matrix Metalloproteinase ◽  
Collagen Type ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Abdominal Aortic ◽  
Collagen Type 1

Objectives: MicroRNA (miR)-1260 was identified to be down-regulated in vascular smooth muscle cells (VSMCs) from human abdominal aortic aneurysm (AAA) tissues in our previous microarray profiling assay. MiR-1260 was predicted to target and down-regulate collagen type 1 alpha 1 (COL1A1), which is closely related to AAA formation, from a bioinformatics analysis. However, the role of miR-1260 in VSMCs for AAA formation still remains uncertain. This study aims to investigate the role of miR-1260 in human VSMCs. Methods: Stable overexpression and knockdown of miR-1260 using lentivirus were performed in VSMCs cultured from human abdominal aortic tissues. Expression of COL1A1 protein was investigated, followed by investigating the expressions of several key components involved in AAA pathogenic features: monocyte chemoattractant protein-1 (MCP-1) for inflammation; matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of matrix metalloproteinase (TIMP)- 1 and TIMP-2 for elastin fragmentation. Apoptosis of VSMCs was also examined. Results: Both COL1A1 and MCP-1 were significantly down-regulated upon miR-1260 overexpression, whereas they were significantly up-regulated upon miR-1260 knockdown. Neither protein expressions of MMP-2, MMP-9, TIMP-1 and TIMP-2 nor apoptosis were significantly different between miR-1260 overexpression/knockdown and corresponding controls. Conclusions: Our findings suggested suppression of miR-1260, which was previously found associated with AAA VSMCs, may promote up-regulation of COL1A1 and MCP-1 in human VSMCs, possibly promoting compensatory collagen synthesis and inflammation for AAA formation.

Sign in / Sign up

Export Citation Format

Share Document