IL-4 stimulates the expression of CXCL-8, E-selectin, VEGF, and inducible nitric oxide synthase mRNA by equine pulmonary artery endothelial cells

Hong, Huixiao; Lavoie-Lamoureux, Anouk; Moran, Kantuta; Lavoie, Jean‐Pierre

doi:10.1152/ajplung.00294.2006

Cited by 43 publications

(32 citation statements)

References 59 publications

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“…induces VCAM-1 expression in cultured endothelial cells (15). Consistent with these data, incubation of human umbilical vein endothelial cells (HUVECs) with 20 ng/ml IL-4 resulted in a time-dependent increase in IL-4 mRNA, as measured by realtime PCR, with peak levels (39.6-fold) occurring at 24 h (Fig.…”

Section: Il-4 Induces Vcam-1 But Not Icam-1 Expression In Cultured Ensupporting

confidence: 81%

“…Activation of the receptor results in Janus kinase 1/2 (JAK-1/2)-dependent tyrosine phosphorylation and subsequent dimerization of signal transducer and activation of transcription 6 (STAT6), which then translocates to the nucleus and binds to consensus sequences (TTCN 3-4 GAA) found within promoters of IL-4-regulated target genes (14,27). Previous studies with endothelial cells have demonstrated that IL-4 induces the expression of CXCL-8, inducible nitric oxide synthase (iNOS) (15), urokinase-type plasminogen activator (u-PA) (46), vascular endothelial growth factor (VEGF) (15), P-selectin (20,32,47), monocyte chemoattractant protein 1 (MCP-1) (39), CCL26 (18), , 15-lipoxygenase (24), and osteoprotegerin (41). In addition, previous studies have shown that IL-4 upregulates the expression of VCAM-1 in endothelial cells (4,10,14,23,26,37,40).…”

mentioning

confidence: 99%

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Genome-Wide Approaches Reveal Functional Interleukin-4-Inducible STAT6 Binding to the Vascular Cell Adhesion Molecule 1 Promoter

Tozawa

Kanki

Suehiro

et al. 2011

Molecular and Cellular Biology

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Section: Il-4 Induces Vcam-1 But Not Icam-1 Expression In Cultured Ensupporting

confidence: 81%

mentioning

confidence: 99%

Genome-Wide Approaches Reveal Functional Interleukin-4-Inducible STAT6 Binding to the Vascular Cell Adhesion Molecule 1 Promoter

Tozawa

Kanki

Suehiro

et al. 2011

Molecular and Cellular Biology

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“…iNOS mRNA levels were significantly increased 8.9-fold and 4.7-fold in response to BCG in 253J and T24 cells, respectively, relative to controls ( Figure 2, p < 0.001). As reported earlier, pretreatment of cells with 1400W inhibited BCG induced iNOS expression [16,17]. Compared to BCG, cells treated with 1400W prior to BCG exposure exhibited significantly decreased iNOS expression (7.5-and 4-fold in 253J and T24 cells, respectively, p<0.0001).…”

Section: Inos Expressionsupporting

confidence: 69%

iNOS expression and NO production contribute to the direct effects of BCG on urothelial carcinoma cell biology

Shah¹,

Zhang²,

Chen³

et al. 2014

Urologic Oncology: Seminars and Original Investigations

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OBJECTIVES-Evidence suggests that oxidative stress occurring as a consequence of inducible nitric oxide synthase/nitric oxide (iNOS/NO) contributes to the biologic effects of Bacille Calmette Guérin (BCG). Objective of the current study is to examine iNOS expression, NO production and the biologic impact of NO, on established intermediate end points for the human urothelial carcinoma cell response to BCG. MATERIALS AND METHODS-Quantitative rt-PCR and real time measurement of NO wasused to assess iNOS and NO production respectively, in two human urothelial carcinoma (UC) cell lines, in response to BCG. The effect of blocking NO production using the specific iNOS inhibitor 1400W was determined for multiple intermediate end points characterizing BCGs direct effects on tumor cell biology. Activation of NF-κB and NRF2 signaling pathways, transactivation of genes including p21, CD54, IL6, IL8, CXCL1, CXCL3, CCL20 and cytotoxicity as measured by vital dye exclusion, lactate dehydrogenase (LDH) release and MTT assay were measured in response to BCG with and without iNOS inhibition.RESULTS-Exposure of UC cells to BCG significantly increased both iNOS expression and NO production. Inhibition of iNOS activity with 1400W significantly inhibited BCG's direct biologic effect on UC cells for all of the end points evaluated.CONCLUSIONS-iNOS expression, NO production and the associated oxidative stress play a central role in the response of UC cells to BCG exposure. Manipulation of oxidative stress may afford an opportunity to enhance the antitumor effects of BCG.

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“…Our results revealed that infected IL-4 -/-mice showed diminished leukocyte adhesion at 3 dpi when compared to infected WT mice. Previous studies have demonstrated that IL-4 regulates expression of adhesion molecules, with an upregulatory effect on vascular cell adhesion molecule-1 (VCAM-1) 22,23 and possibly on Pselectin 24,25 and a downregulatory effect on E-selectin 26,27 . It has also been reported that IL-4 can act synergistically with other cytokines, such as IL-1β and TNF-α, in order to promote lymphocyte binding to cultured microvascular endothelial cells 28,29 .…”

Section: Discussionmentioning

confidence: 99%

Role of IL-4 in an experimental model of encephalitis induced by intracranial inoculation of herpes simplex virus-1 (HSV-1)

Vilela

Campos

Mansur³

et al. 2011

Arq. Neuro-Psiquiatr.

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Herpes simplex virus-1 (HSV-1) is a pathogen that may cause severe encephalitis in humans. In this study, we aimed to investigate the role of interleukin-4 (IL-4) in a model of HSV-1 brain infection. IL-4 knockout (IL-4 -/-) and wild type (WT) C57BL/6 mice were inoculated with 10 4 plaque-forming units of HSV-1 by the intracranial route. Histopathologic analysis revealed a distinct profile of infiltrating cells at 3 days postinfection (dpi). Infected WT mice presented mononuclear inflammatory cells while IL-4 -/-mice developed meningoencephalitis with predominance of neutrophils. IL-4 -/-mice had diminished leukocyte adhesion at 3 dpi when compared to infected WT animals in intravital microscopy study. Conversely no differences were found in cerebral levels of CXCL1, CXCL9, CCL3, CCL5 and TNF-α between WT and IL-4 -/-infected mice. IL-4 may play a role in the recruitment of cells into central nervous system in this acute model of severe encephalitis caused by HSV-1. Key words: herpes simplex virus type 1, IL-4, neuroinflammation.Papel da IL-4 em modelo experimental de encefalite induzida pela inoculação intracraniana do herpes simplex vírus-1 (HSV-1) RESUMO O vírus herpes simplex-1 (HSV-1) é um patógeno que pode causar encefalite grave em humanos. Neste estudo, buscamos investigar o papel da interleucina-4 (IL-4) no modelo de infecção intracerebral por HSV-1. Camundongos C57BL/6 selvagens (WT) e deficientes no gene IL-4 (IL-4 -/-) foram inoculados com 10 4 unidades formadoras de placas de HSV-1 por via intracraniana. A análise histopatológica revelou um padrão distinto de infiltrado leucocitário. Camundongos WT infectados apresentaram infiltrado de células mononucleares, enquanto camundongos IL-4 -/-desenvolveram meningoencefalite com predomínio de neutrófilos 3 dias pós-infecção (dpi). Animais IL-4 -/-tiveram menor adesão de leucócitos 3 dpi quando comparados aos animais WT infectados à microscopia intravital. Em contrapartida, não foram encontradas diferenças nos níveis cerebrais de CXCL1, CXCL9, CCL3, CCL5 e TNF-α entre camundongos WT e IL-4 -/-infectados. Esses resultados sugerem que IL-4 pode desempenhar um papel no recrutamento de células no sistema nervoso central neste modelo agudo de encefalite grave causada pelo HSV-1. Palavras-chave: vírus herpes simplex tipo 1, IL-4, neuroinflamação. Correspondence

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IL-4 stimulates the expression of CXCL-8, E-selectin, VEGF, and inducible nitric oxide synthase mRNA by equine pulmonary artery endothelial cells

Abstract: stimulates the expression of CXCL-8, E-selectin, VEGF, and inducible nitric oxide synthase mRNA by equine pulmonary artery endothelial cells.

Cited by 43 publications

References 59 publications

Genome-Wide Approaches Reveal Functional Interleukin-4-Inducible STAT6 Binding to the Vascular Cell Adhesion Molecule 1 Promoter

Genome-Wide Approaches Reveal Functional Interleukin-4-Inducible STAT6 Binding to the Vascular Cell Adhesion Molecule 1 Promoter

iNOS expression and NO production contribute to the direct effects of BCG on urothelial carcinoma cell biology

Role of IL-4 in an experimental model of encephalitis induced by intracranial inoculation of herpes simplex virus-1 (HSV-1)

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