Cytokine-induced cell surface expression of adhesion molecules in vascular endothelial cellsIn vitro

Chen, H; Liu, C; Sun, Shan; Mei, Yuan-wu; E-tang, Tong

doi:10.1007/bf02888042

Cited by 12 publications

(4 citation statements)

References 8 publications

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“…Proinflammatory cytokines are well known to regulate the expression of adhesion molecules in various cells (Chen et al ., 2001; Kwon et al ., 2007). To examine the effect of SB-657510 on the expression of cytokines in endothelial cells, we investigated the mRNA expression of cytokines (IL-1β, IL-6, IL-8, and TNF-β) in EA.hy926 cells.…”

Section: Resultsmentioning

confidence: 99%

Inhibitory Effect of an Urotensin II Receptor Antagonist on Proinflammatory Activation Induced by Urotensin II in Human Vascular Endothelial Cells

Park¹,

Lee²,

Kim³

et al. 2013

Biomolecules and Therapeutics

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In this study, we investigated the effects of a selective urotensin II (UII) receptor antagonist, SB-657510, on the inflammatory response induced by UII in human umbilical vein endothelial cells (EA.hy926) and human monocytes (U937). UII induced inflammatory activation of endothelial cells through expression of proinflammatory cytokines (IL-1β and IL-6), adhesion molecules (VCAM-1), and tissue factor (TF), which facilitates the adhesion of monocytes to EA.hy926 cells. Treatment with SB-657510 significantly inhibited UII-induced expression of IL-1β, IL-6, and VCAM-1 in EA.hy926 cells. Further, SB-657510 dramatically blocked the UII-induced increase in adhesion between U937 and EA.hy926 cells. In addition, SB-657510 remarkably reduced UII-induced expression of TF in EA.hy926 cells. Taken together, our results demonstrate that the UII antagonist SB-657510 decreases the progression of inflammation induced by UII in endothelial cells.

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Section: Resultsmentioning

confidence: 99%

Inhibitory Effect of an Urotensin II Receptor Antagonist on Proinflammatory Activation Induced by Urotensin II in Human Vascular Endothelial Cells

Park¹,

Lee²,

Kim³

et al. 2013

Biomolecules and Therapeutics

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“…Furthermore, data revealed the circulating levels of TNF-α in both groups of patients were strongly correlated with each of sICAM-1 and sVCAM-1 values in these patients. These findings indicate that TNF-α might directly induce the expression of ICAM-1 and VCAM-1 in vascular endothelial cells 36. Moreover, correlation was found between monocyte adhesion molecules CD11a, CD11b and CD49d and each of sICAM-1 and sVCAM-1 which suggest the useful use of these soluble markers as an indicator of enhanced monocyte recruitment to the liver.…”

Section: Discussionmentioning

confidence: 70%

Monocyte Adhesion Molecules Expression in Patients With Chronic Hepatitis C and Liver Cirrhosis

El-Bassiouni¹,

Mahmoud²,

Ahwani³

et al. 2013

Mediterr J Hematol Infect Dis

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BackgroundChronic viral hepatitis is histologically characterized by predominantly periportal infiltration of mononuclear cells, including lymphocytes and monocytes/macrophages. Intralobular infiltration of these inflammatory cells is an ominous sign of deterioration and a criterion for disease activity.ObjectiveTo assess the monocyte inflammatory milieu, monocytes adhesion molecules, their endothelial receptors, cytokines and chemokines in patients with HCV induced chronic liver disease, in an attempt to clarify the role of blood monocytes in induction of inflammation and fibrogenesis in chronic hepatitis C liver disease.Subjects and MethodsThe current study included 60 patients with chronic liver disease categorized into 2groups: Patients chronic hepatitis C (CHC) and patients with liver cirrhosis (LC), 15 patients each; 15 healthy subjects were included as normal controls. Immunophenotype characterization was carried out by flowcytometric analysis for identification of CD11a, CD11b and CD49d monocyte surface antigen expression in different groups studied. The circulating levels of the soluble adhesion molecules (sE-selectin, sICAM-1 and sVCAM-1), cytokines (TNF-α and IL-1) and chemokines (MCP-1) were also assessed by immunoassays.ResultsData demonstrated a significant increase (p<0.01) in the surface expression of CD11a on peripheral blood monocytes and in the circulating levels sE-selectins, sICAM-1, sVCAM-1 and TNF-α in both groups of patients compared to healthy subjects. Data also revealed a significant increase (p<0.01) in the surface expression of each of CD11b and CD49d on peripheral blood monocytes and in the circulating levels sICAM-1, sVCAM-1 and TNF-α in patients with LC compared to those with CHC. Moreover, data demonstrated that the increase in surface antigen expression of each CD11a (p<0.01), CD11b (p<0.05) and CD49d (p<0.01) on circulating peripheral blood monocytes is positively correlated with the increase in the circulating levels of each of sICAM-1 and sVCAM-1 in the both groups of patients.ConclusionsThese findings suggest that the modulation of monocyte-subset recruitment into the liver via adhesion molecules or cytokines/cytokine receptors may represent promising approaches for therapeutic interventions in human liver fibrosis. Measurement of serum soluble adhesion molecules may be useful for monitoring progression of liver inflammation and fibrosis during CHC.

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“…In the current investigation, IL-1beta remained elevated at all time points, which may be related to sustained inflammasome activation, thus explaining the effect of persistent inflammation on metabolic memory. This is because this cytokine increases the expression of cell adhesion molecules, such as vascular cellular adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemoattractant protein-1 (MCP-1), in endothelial vessel cells, which are responsible for recruiting macrophages [ 25 , 26 , 27 ].…”

Section: Discussionmentioning

confidence: 99%

The Prolonged Activation of the p65 Subunit of the NF-Kappa-B Nuclear Factor Sustains the Persistent Effect of Advanced Glycation End Products on Inflammatory Sensitization in Macrophages

Assis,

Amendola,

Okamoto

et al. 2024

IJMS

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Advanced glycation end products (AGEs) prime macrophages for lipopolysaccharide (LPS)-induced inflammation. We investigated the persistence of cellular AGE-sensitization to LPS, considering the nuclear content of p50 and p65 nuclear factor kappa B (NFKB) subunits and the expression of inflammatory genes. Macrophages treated with control (C) or AGE-albumin were rested for varying intervals in medium alone before being incubated with LPS. Comparisons were made using one-way ANOVA or Student t-test (n = 6). AGE-albumin primed macrophages for increased responsiveness to LPS, resulting in elevated levels of TNF, IL-6, and IL-1beta (1.5%, 9.4%, and 5.6%, respectively), compared to C-albumin. TNF, IL-6, and IL-1 beta secretion persisted for up to 24 h even after the removal of AGE-albumin (area under the curve greater by 1.6, 16, and 5.2 times, respectively). The expressions of Il6 and RelA were higher 8 h after albumin removal, and Il6 and Abca1 were higher 24 h after albumin removal. The nuclear content of p50 remained similar, but p65 showed a sustained increase (2.9 times) for up to 24 h in AGE-albumin-treated cells. The prolonged activation of the p65 subunit of NFKB contributes to the persistent effect of AGEs on macrophage inflammatory priming, which could be targeted for therapies to prevent complications based on the AGE–RAGE–NFKB axis.

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Cytokine-induced cell surface expression of adhesion molecules in vascular endothelial cellsIn vitro

Cited by 12 publications

References 8 publications

Inhibitory Effect of an Urotensin II Receptor Antagonist on Proinflammatory Activation Induced by Urotensin II in Human Vascular Endothelial Cells

Inhibitory Effect of an Urotensin II Receptor Antagonist on Proinflammatory Activation Induced by Urotensin II in Human Vascular Endothelial Cells

Monocyte Adhesion Molecules Expression in Patients With Chronic Hepatitis C and Liver Cirrhosis

The Prolonged Activation of the p65 Subunit of the NF-Kappa-B Nuclear Factor Sustains the Persistent Effect of Advanced Glycation End Products on Inflammatory Sensitization in Macrophages

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