Vascular Endothelial Growth Factor Expression of Intercellular Adhesion Molecule 1 (ICAM-1), Vascular Cell Adhesion Molecule 1 (VCAM-1), and E-selectin through Nuclear Factor-κB Activation in Endothelial Cells

Kim, Injune; Moon, Sang-Ok; Kim, Sung Hoon; Kim, Hyung Jin; Koh, Young Soon; Koh, Gou Young

doi:10.1074/jbc.m009705200

Cited by 684 publications

(519 citation statements)

References 35 publications

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“…To ensure specificity of probe binding, controls using a 50-fold excess of unlabeled (cold) and mutant scrambled oligonucleotides were added to the nuclear samples and incubated for 10 min before labeled oligonucleotide was added. Our results indicating that 50 nM wortmannin suppressed VEGF-induced NF-jB binding, which is in contrast with some reports 34,35 but consistent with others, 17,36 demonstrate that NF-jB is dependent on PI3 kinase/Akt signaling in our system.…”

Section: Resultscontrasting

confidence: 57%

Green tea catechin, epigallocatechin‐3‐gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex

Rodriguez

Guo

Liu

et al. 2005

Intl Journal of Cancer

116

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A potential mechanism by which green tea may prevent cancer development is through the inhibition of angiogenesis. We have shown previously that the green tea catechin, epigallocatechin gallate (EGCG), inhibits endothelial cell tube formation through the inhibition of vascular endothelial growth factor (VEGF)-induced Akt activation and vascular endothelial (VE)-cadherin phosphorylation. Furthermore, EGCG can suppress oxidant-induced production of the proangiogenic cytokine interleukin (IL)-8. To further elucidate the antiangiogenic mechanisms of EGCG, we investigated its regulation of other molecular processes in VEGFinduced signaling in human umbilical vein endothelial cells (HUVECs). We show that EGCG at physiological doses (0.5-10 lM) markedly inhibits the formation of a vascular endothelial growth factor receptor 2 complex formed upon the binding of its ligand VEGF. This disruption results in a significant and dosedependent decrease in PI3-kinase activity. Electrophoretic mobility shift assay revealed that EGCG decreased the PI3 kinasedependent activation and DNA-binding ability of NF-jB, likely acting through decreasing phosphorylation and degradation of IjB. VEGF-induced IL-8 production at the mRNA (real time RT-PCR) and protein levels (ELISA) are also suppressed with EGCG. These results suggest a novel mechanism for green tea's anticancer effects where EGCG can abrogate VEGF signaling by interfering with the formation of a receptor complex, resulting in attenuated mitogenic and angiogenic signaling. ' 2005 Wiley-Liss, Inc.

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Section: Resultscontrasting

confidence: 57%

Green tea catechin, epigallocatechin‐3‐gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex

Rodriguez

Guo

Liu

et al. 2005

Intl Journal of Cancer

116

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“…In contrast, it has been suggested that the NO-dependent pathway is not involved in VEGF-induced mRNA expression of VCAM-1 in human umbilical vein endothelial cells (HUVECS). 11 The results of this study indicate that sunitinib, a promiscuous drug against multiple tyrosine kinases, affects Ang-2 signaling, which may reflect an additional beneficial effect of sunitinib in patients with mRCC. In these patients, circulating Ang-2 levels are elevated and are associated with the extent of disease.…”

Section: Discussionmentioning

confidence: 76%

“…7 In response to VEGF, the endothelium is activated and several proteins are expressed by endothelial cells including vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), von Willebrand factor (vWF), angiopoietin-2 (Ang-2) and Tie-2 (Tie-2). [8][9][10][11] VCAM-1 and ICAM-1 are adhesion molecules and their soluble ectodomains (sVCAM-1 and sICAM-1) can be proteolytically released from the endothelial cell surface into the circulation. [12][13][14] Next to upregulation of VCAM-1 and ICAM-1, VEGF is also known to activate exocytosis of intracellular secretory granules in endothelial cells, the so-called Weibel-Palade bodies, thereby releasing vasoactive substances, including von Willebrand factor (vWF) and Ang-2.…”

mentioning

confidence: 99%

Sunitinib‐induced changes in circulating endothelial cell‐related proteins in patients with metastatic renal cell cancer

Veldt

Vroling

Haas

et al. 2011

Intl Journal of Cancer

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Vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors are effective agents in the treatment of metastatic renal cell cancer (mRCC). We here investigated whether inhibition of VEGFR signalin by sunitinib causes changes in plasma proteins associated with tumor endothelium. Forty-three patients with mRCC received sunitinib 50 mg/day in a 4-weeks on 2-weeks off schedule. Sequential plasma samples were obtained before treatment (C1D1), on C1D14, on C1D28, and on C2D1 before start of cycle 2. Plasma levels were assessed for VEGF, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular cell adhesion molecule-1 (sICAM-1), von Willebrand factor (vWF), circulating angiopoietin-2 (Ang-2) and soluble Tie-2 (sTie-2). Total tumor burden was calculated at baseline and at first evaluation. Progression-free survival (PFS) and overall survival (OS) were determined. Tumor burden was positively associated with baseline circulating Ang-2 [Spearman's rho (q) 5 0.378, p 5 0.028] and vWF (q 5 0.417, p 5 0.008). During sunitinib treatment, circulating Ang-2 and sTie-2 significantly decreased (p < 0.001 for both), plasma levels of sVCAM-1 and VEGF significantly increased (p 5 0.022 and p < 0.001), whereas those of sICAM-1 and vWF remained stable. These protein changes had recovered on C2D1. The reduction in circulating Ang-2 levels on C1D28 was positively correlated with the percentage decrease in tumor burden (q 5 0.605; p 5 0.002). Baseline protein levels and subsequent changes were not associated with PFS or OS. In conclusion, sunitinib-induced changes in Ang-2, sTie-2, sVCAM-1 and VEGF are related to the administration schedule, while reduction in Ang-2 is also associated with decrease in tumor burden.

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“…PMA/Io mimics the phospholipase C-driven activation of protein kinase C and cytosolic Ca 2+ increase and induces activation of NF-B, NFAT and AP-1. NF-B is of special interest in endothelial cells since it drives the expression of important adhesion molecules, such as ICAM-1, which recruit blood monocytes to atherosclerotic lesions [6]. NFAT cooperated with NF-B to regulate thrombin-induced ICAM-1 gene expression by binding to the intronic NF-κB site in the ICAM-1 gene [7].…”

mentioning

confidence: 99%

SIRT1 suppresses PMA and ionomycin-induced ICAM-1 expression in endothelial cells

Jia

Gao

Chen

et al. 2012

Sci. China Life Sci.

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Intercellular adhesion molecule-1 (ICAM-1) plays an important role in the recruitment of leukocytes to the endothelium, which causes inflammation and initiation of atherosclerosis. We have previously shown that endothelium-specific over-expression of class III deacetylase SIRT1 decreases atherosclerosis. We therefore addressed the hypothesis that SIRT1 suppresses ICAM-1 expression in the endothelial cells. Here, we found that expression of SIRT1 and ICAM-1 was significantly induced by PMA and ionomycin (PMA/Io) in human umbilical vein endothelial cells (HUVECs). Adenovirus-mediated over-expression of SIRT1 significantly inhibited PMA/Io-induced ICAM-1 expression in HUVECs. Knockdown of SIRT1 by RNA interference (RNAi) resulted in increased expression of ICAM-1 in HUVECs. Luciferase report assay showed that over-expression of SIRT1 suppressed ICAM-1 promoter activity both in basic and in PMA/Io-induced conditions. We further found that SIRT1 was involved in transcription complex binding on the ICAM-1 promoter by chromatin immunoprecipitation (ChIP) assays. Furthermore, SIRT1 RNAi increased NF-κB p65 binding ability to the ICAM-1 promoter by ChIP assays. Overall, these data suggests that SIRT1 inhibits ICAM-1 expression in endothelial cells, which may contribute to its anti-atherosclerosis effect. SIRT1, ICAM-1, PMA and ionomycin Citation:Jia Y Y, Gao P, Chen H Z, et al. SIRT1 suppresses PMA and ionomycin-induced ICAM-1 expression in endothelial cells .

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Vascular Endothelial Growth Factor Expression of Intercellular Adhesion Molecule 1 (ICAM-1), Vascular Cell Adhesion Molecule 1 (VCAM-1), and E-selectin through Nuclear Factor-κB Activation in Endothelial Cells

Abstract: The adhesive properties of the endothelium, the single-cell lining of the cardiovascular system, are central to its physiology and pathophysiology (1, 2). In health, the luminal endothelial cell surface is a relatively nonadhesive and nonthrombo-

Cited by 684 publications

References 35 publications

Green tea catechin, epigallocatechin‐3‐gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex

Green tea catechin, epigallocatechin‐3‐gallate, inhibits vascular endothelial growth factor angiogenic signaling by disrupting the formation of a receptor complex

Sunitinib‐induced changes in circulating endothelial cell‐related proteins in patients with metastatic renal cell cancer

SIRT1 suppresses PMA and ionomycin-induced ICAM-1 expression in endothelial cells

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