scholarly journals The Integrin α9β1 Mediates Adhesion to Activated Endothelial Cells and Transendothelial Neutrophil Migration through Interaction with Vascular Cell Adhesion Molecule-1

1999 ◽  
Vol 145 (2) ◽  
pp. 413-420 ◽  
Author(s):  
Yasuyuki Taooka ◽  
John Chen ◽  
Ted Yednock ◽  
Dean Sheppard
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Umbilical Vein ◽  
Neutrophil Migration ◽  
Peptide Sequence ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Tenascin C ◽  
Umbilical Vein Endothelial Cells ◽  
Factor Α

The integrin α9β1 has been shown to be widely expressed on smooth muscle and epithelial cells, and to mediate adhesion to the extracellular matrix proteins osteopontin and tenascin-C. We have found that the peptide sequence this integrin recognizes in tenascin-C is highly homologous to the sequence recognized by the closely related integrin α4β1, in the inducible endothelial ligand, vascular cell adhesion mole-cule-1 (VCAM-1). We therefore sought to determine whether α9β1 also recognizes VCAM-1, and whether any such interaction would be biologically significant. In this report, we demonstrate that α9β1 mediates stable cell adhesion to recombinant VCAM-1 and to VCAM-1 induced on human umbilical vein endothelial cells by tumor necrosis factor-α. Furthermore, we show that α9β1 is highly and selectively expressed on neutrophils and is critical for neutrophil migration on VCAM-1 and tenascin-C. Finally, α9β1 and α4 integrins contribute to neutrophil chemotaxis across activated endothelial monolayers. These observations suggest a possible role for α9β1/VCAM-1 interactions in extravasation of neutrophils at sites of acute inflammation.

Rhein Inhibits the Expression of Vascular Cell Adhesion Molecule 1 in Human Umbilical Vein Endothelial Cells with or without Lipopolysaccharide Stimulation

2013 ◽  
Vol 41 (03) ◽  
pp. 473-485 ◽  
Author(s):  
Gang Hu ◽  
Jiang Liu ◽  
Yong-Zhan Zhen ◽  
Jie Wei ◽  
Yue Qiao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Umbilical Vein ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Vascular Cell Adhesion Molecule ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1

Reducing the expression of endothelial cell adhesion molecules (ECAMs) is known to decrease inflammation-induced vascular complications. In this study, we explored whether rhein can reduce the inflammation-induced expression of ECAMs in human umbilical vein endothelial cells (HUVECs) with or without lipopolysaccharide (LPS) stimulation. HUVECs were treated with different concentrations of rhein with or without 2.5 μg/ml LPS stimulation. Cell viability was assayed using the MTT method. Real-time PCR and Western blot analysis were used to measure the transcription and expression levels of ECAMs, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-SELECTIN and related signaling proteins. The results indicated that rhein (0–20 μmol/L) and LPS (0–10 μg/ml) had no effect on the viability of HUVECs. LPS could promote the expression of VCAM-1, ICAM-1 and E-SELECTIN. Rhein appeared to target VCAM-1, ICAM-1 and E-SELECTIN, with the transcription and expression of all three factors being reduced by the rhein treatment (10 and 20 μmol/L). The transcription and expression of VCAM-1 were also reduced by treatment with rhein (10 and 20 μmol/L) in the presence of LPS stimulation. In conclusion, rhein treatment reduced the expression of VCAM-1 in HUVECs via a p38-dependent pathway.

Febuxostat Attenuates the Induction of Vascular Cell Adhesion Protein 1 by TNF-α in Human Umbilical Vein Endothelial Cells

Pharmacology ◽  
2020 ◽  
pp. 1-7
Author(s):  
Yasuhiro Suzuki ◽  
Mari Deguchi ◽  
Airi Furuya ◽  
Sayuki Kato ◽  
Shoichiro Ohta
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Umbilical Vein ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Adhesion Protein ◽  
Human Umbilical Vein ◽  
Cell Adhesion Protein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

In a randomized trial, higher all-cause and cardiovascular mortality was observed in treatment with febuxostat than with allopurinol in patients with coexisting gout and serious cardiovascular conditions. In this study, we focus on an intervention of febuxostat or allopurinol as an anti-inflammatory treatment to reduce the transcription of nuclear factor-kappa B (NF-κB) and production of relevant inflammatory factors. We evaluated the effect of febuxostat on vascular cell adhesion protein 1 (VCAM-1) induction in cultured human umbilical vein endothelial cells (HUVECs). Cells were exposed to tumor necrosis factor (TNF)-α (10 ng/mL) treatment for 24 h. Febuxostat or allopurinol (0.1–100 μM) was added to the bath medium 15 min before TNF-α treatment. VCAM-1 levels in HUVECs increased after 24-h TNF-α treatment (<i>n</i> = 4). Febuxostat and allopurinol significantly suppressed VCAM-1 induced by treatment with TNF-α in a dose-dependent manner (<i>p</i> &#x3c; 0.05, <i>n</i> = 4). Furthermore, these drugs suppressed the NF-κB protein levels in the nucleus 4 h after TNF-α treatment (<i>n</i> = 3 or 4). Our results suggest that TNF-α induces VCAM-1 production via NF-κB, which can be blocked by febuxostat or allopurinol. The effect of febuxostat treatment on cardiovascular events may be associated with protection against the infiltration of lymphocytes or monocytes through VCAM-1 induction in inflamed endothelial cells such as arterial sclerosis.

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