Activation of Adenosine-receptor-enhanced iNOS mRNA Expression by Gingival Epithelial Cells

Murakami, Shinya; Yoshimura, Naoko; Koide, Hiroko; Watanabe, Junko; Takedachi, Masahide; Terakura, Mami; Yanagita, Manabu; Hashikawa, Tomoko; Saho, Teruyuki; Shimabukuro, Yoshio; Okada, Hiroshi

doi:10.1177/154405910208100403

Cited by 38 publications

(29 citation statements)

References 25 publications

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“…The effect of the CaR on iNOS is not a nonspecific event caused by activation of any GPCR, since activation of a functional G␣ q-11 -coupled purinergic receptor in these cells by ADP␤S (a nondegradable form of ADP) failed to alter iNOS expression in the H-500 cells. Activation of ADP receptors (like the CaR, a GPCR coupled to G␣ q-11 ) has been reported to upregulate the level of iNOS mRNA in human gingival epithelial cells (22). In the same cells, additional studies showed that IL-15 enhanced iNOS expression at both the mRNA and protein levels, similar to our study (39).…”

Section: Discussionsupporting

confidence: 87%

Calcium-sensing receptor activation induces nitric oxide production in H-500 Leydig cancer cells

Tfelt-Hansen

Ferreira²,

Yano³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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Nitric oxide (NO) is a versatile second messenger. NO is produced by Leydig cells, where NO is a negative regulator of steroidogenesis. In cancer cells, NO is thought to have mutagenic and proliferative effects. We have previously shown that the calcium-sensing receptor (CaR) has promalignant effects in rat H-500 Leydig cancer cells, a model for humoral hypercalcemia of malignancy. Calcium, the major physiological ligand of the CaR, is a recognized intracellular cofactor in the process of NO production by virtue of its positive modulation of neuronal and endothelial nitric oxide synthase (NOS), but importantly, not of inducible (i) NOS activity. iNOS activity is regulated by changes in its expression level. Therefore, we investigated whether CaR activation changes iNOS expression. We found that high extracellular calcium (Ca[Formula: see text]) upregulates the level of mRNA for iNOS, whereas no change was seen in neuronal or endothelial NOS, as assessed by microarray and real-time PCR, respectively. The high Ca[Formula: see text]-induced iNOS upregulation was also detected by Northern and Western blotting. By quantitative real-time PCR, we showed that calcium maximally upregulates iNOS at 18 h. The effect of calcium was abolished by overexpression of a dominant-negative CaR (R185Q), confirming that the effect of Ca[Formula: see text] was mediated by the CaR. Cells treated with high calcium had higher NO production than those treated with low calcium, as detected with the NO-specific DAF2-AM dye. This was confirmed in single-cell fluorescence determinations using confocal microscopy. In conclusion, high calcium upregulates the levels of iNOS mRNA and protein as well as NO production in H-500 cells, and the effect of Ca[Formula: see text] on iNOS expression is mediated by the CaR.

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Section: Discussionsupporting

confidence: 87%

Calcium-sensing receptor activation induces nitric oxide production in H-500 Leydig cancer cells

Tfelt-Hansen

Ferreira²,

Yano³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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“…Simian virus‐40 antigen‐mediated, immortalized gingival epithelial cell lines, epi 4 and OBA‐9 , were maintained in Humedia‐KG2 medium (Kurabo, Osaka, Japan) containing 0.5 μg/mL hydrocortisone, 10 μg/mL insulin, 0.4% v/v bovine pituitary extract, 0.1 ng/mL human epidermal growth factor, 50 μg/mL gentamycin and 50 ng/mL amphotericin B. For analysis, cells were cultured in Humedia‐KB2 (Kurabo) medium containing 50 μg/mL gentamycin and 50 ng/mL amphotericin B.…”

Section: Methodsmentioning

confidence: 99%

Hypoxia‐inducible factor‐1α inhibits interleukin‐6 and ‐8 production in gingival epithelial cells during hypoxia

Takedachi

Iyama

Sawada

et al. 2016

J of Periodontal Research

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inducible factor-1a inhibits interleukin-6 and -8 production in gingival epithelial cells during hypoxia.Background and Objective: Hypoxia has been widely studied in inflammatory diseases as it can modulate the inflammatory response, mainly via the hypoxiainducible factor (HIF). However, little is known about the effects of hypoxia and the role of HIF in the inflammatory responses to periodontitis. In this study, we focused on the gingival epithelium that is exposed to relatively low levels of oxygen. We investigated whether hypoxic conditions have an impact on inflammatory responses in human gingival epithelial cells (HGECs).

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“…The human gingival epithelial cell line epi 4 (18) was used in this study. The cells were maintained in Humedia‐KG2 (Kurabo, Osaka, Japan) supplemented with 0.5 μg ml −1 of hydrocortisone, 10 μg ml −1 of insulin, 0.4% (v/v) bovine pituitary extract, 0.1 ng ml ‐1 of human epidermal growth factor, 50 μg ml −1 of gentamicin, and 50 ng ml −1 of amphotericin B (all from Kurabo).…”

Section: Methodsmentioning

confidence: 99%

Effect of interleukin-17 on the expression of chemokines in gingival epithelial cells

Takahashi

Okui

Tabeta

et al. 2011

European Journal of Oral Sciences

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The role of interleukin (IL)-17 in cellular communication in inflammation has been well described, and a positive correlation between the severity of periodontitis and the level of IL-17 was reported. Although epithelial cells are a major target of IL-17, little is known about the effect of IL-17 on the production of chemokines by human gingival epithelial cells (HGECs). We evaluated the effects of IL-17 on the expression of CXCL8 and CCL2 by HGECs using quantitative real-time PCR and ELISA. In addition, the role of the nuclear factor (NF)-κB signalling pathway in the IL-17-mediated expression of chemokines was assessed using a specific inhibitor. Stimulation with IL-17 up-regulated the expression of CXCL8 mRNA but not of CCL2 mRNA in HGECs, whereas tumour necrosis factor-α (TNF-α) elevated the expression of mRNA for both chemokines. Stimulation with IL-17 up-regulated the secretion of CXCL8 protein, but not the secretion of CCL2 protein. The effect of IL-17 on CXCL8 production was suppressed using an anti-IL-17R Ig, suggesting a role for a specific receptor-ligand interaction. Inhibition of the NF-κB signalling pathway demonstrated that NF-κB activation is required for the CXCL8 expression in HGECs. In conclusion, IL-17 is involved in the regulation of the innate immune response in HGECs by inducing CXCL8 production.

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Activation of Adenosine-receptor-enhanced iNOS mRNA Expression by Gingival Epithelial Cells

Cited by 38 publications

References 25 publications

Calcium-sensing receptor activation induces nitric oxide production in H-500 Leydig cancer cells

Calcium-sensing receptor activation induces nitric oxide production in H-500 Leydig cancer cells

Hypoxia‐inducible factor‐1α inhibits interleukin‐6 and ‐8 production in gingival epithelial cells during hypoxia

Effect of interleukin-17 on the expression of chemokines in gingival epithelial cells

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