Modulation of inducible nitric oxide synthase induction by prostaglandin E2 in macrophages: distinct susceptibility in murine J774 and RAW 264.7 macrophages☆

Lina, Wan Wan; Chen, Bing Chang; Hsu, Yu Wen; Lee, Chi-Ming; Shyue, Song Kun

doi:10.1016/s0090-6980(99)00023-4

Cited by 27 publications

(18 citation statements)

References 37 publications

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“…In some studies NO increased PGE 2 synthesis [19,20] whereas in others, NO inhibited PGE 2 synthesis [21,22]. There are also reports of PGE 2 modulating NO synthesis: increasing [23] or decreasing [24,25].…”

Section: Discussionmentioning

confidence: 99%

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Cross-Regulation of iNOS and COX-2 by its Products in Murine Macrophages Under Stress Conditions

Prestes-Carneiro

Shio

Fernandes

et al. 2007

Cell Physiol Biochem

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Exposure of macrophages to heat shock induces rapid synthesis of heat shock proteins (HSPs) which are important for cell homeostasis. Prostaglandins (PGs) and nitric oxide (NO) are important cell regulatory molecules. We have therefore investigated the interactions between these molecules in the LPSinduced expression of iNOS and COX-2 and in the mitochondrial activity of macrophages. Cultures of the murine macrophage cell line, J774, were exposed to heat shock (43°C, 30min) and stimulated with LPS (1 µg/ml), concomitantly or after 8h of cell recovery. NO production was measured by Griess reaction; PGE 2 by ELISA; HSP70, iNOS and COX-2 by immunobloting; mitochondrial activity by MTT assay. Heat shock induced HSP70, but not iNOS or COX-2 whereas LPS induced iNOS and COX-2 but not HSP70. When heat shock and LPS were given concomitantly, iNOS but not COX-2 expression was reduced. When a period of 8h was given between heat shock and LPS stimulation, iNOS, COX-2, PGE 2 and NO levels were significantly increased. Under these conditions, the expression of COX-2 was reduced by L-NAME (NOsynthesis inhibitor) and of iNOS by nimesulide (PGssynthesis inhibitor). Such cross-regulation was not observed in cells at 37°C. These treatments significantly reduced MTT levels in cells at 37°C but not in cells submitted to heat shock. These results suggest that HSPs and cross-regulation of iNOS and COX-2 by their products might be of relevance in the control of cell homeostasis during stress conditions.

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Section: Discussionmentioning

confidence: 99%

“…NO was shown to either increase [19,20] or decrease [21,22] prostaglandin synthesis. Prostaglandins were reported to increase [23] or decrease [24,25] NO synthesis. However, interaction among prostaglandins and NO in cells submitted to heat shock were not reported.…”

Section: Introductionmentioning

confidence: 99%

Cross-Regulation of iNOS and COX-2 by its Products in Murine Macrophages Under Stress Conditions

Prestes-Carneiro

Shio

Fernandes

et al. 2007

Cell Physiol Biochem

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“…phages, PGE 2 action is associated with increased cAMP production. Our previous results [25] have demonstrated that UTP in J774 macrophages dramatically potentiates LPS-induced PGE 2 release, which is partially dependent on protein kinase A activation and exhibits positive feedback mechanism. Thus it is interesting to explore whether UTP might modulate IL-6 production subsequent to the enhanced release of PGE 2 .…”

Section: Discussionmentioning

confidence: 82%

“…Figure 3a and b shows that L-NAME at 300 ÌM inhibited NO formation induced by LPS alone or LPS plus UTP by 67 B 11 or 88 B 10% (n = 3), but did not affect IL-6 synthesis. Moreover, NS-398 (10 nM) and indomethacin (0.3 ÌM) at concentrations that abolished COX-2-mediated PGE 2 release [25] inhibited IL-6 release in response to LPS by 38 B 8 and 31 B 8% (n = 3), respectively. Under both treatments, UTP still enhanced IL-6 release to a similar extent (fig.…”

Section: Pge 2 Positively Regulates Il-6 Synthesismentioning

confidence: 93%

Potentiation of Lipopolysaccharide-Induced IL-6 Release by Uridine Triphosphate in Macrophages: Cross-Interaction with Cyclooxygenase-2-Dependent Prostaglandin E<sub>2</sub> Production

Chen

Lin²

1999

J Biomed Sci

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Our previous study has demonstrated the potentiation by uridine triphosphate (UTP) of nitric oxide (NO) and prostaglandin E₂ (PGE₂) production in lipopolysaccharide (LPS)-stimulated murine J774 macrophages. In this study, we found that the amount of interleukin-6 (IL-6) release in response to LPS stimulation was greatly enhanced in the presence of UTP. This enhancement exhibited concentration dependence and occurred after 8 h of treatment with LPS. RT-PCR analysis indicated that the steady-state level of IL-6 mRNA induced by LPS was apparently increased upon co-addition of UTP. The potentiation by UTP was inhibited by the treatment with U73122 (a phosphatidylinositol-phospholipase C inhibitor), BAPTA/AM (an intracellular Ca²⁺ chelator), KN-93 (a selective inhibitor of calmodulin-dependent protein kinase) or PDTC (a nuclear factor κB inhibitor). To understand the cross-regulation among NO, PGE₂ and IL-6, all of which are dramatically induced after LPS stimulation, the effects of L-NAME (a nitric oxide synthase inhibitor), indomethacin (a cyclooxygenase inhibitor), NS-398 (a cycloxygenase-2 inhibitor) and IL-6 antibody were tested. The results revealed the positive regulation between PGE₂ and IL-6 synthesis because NS-398 and indomethacin inhibited LPS plus UTP-induced IL-6 release, and IL-6 antibody attenuated LPS plus UTP-induced PGE₂ release. Taken together these results reinforce the role of UTP as a regulatory element in inflamed sites by demonstrating the capacity of this nucleotide to potentiate LPS-induced release of inflammatory mediators.

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“…In contrast, COX-2 expression is induced by growth factors, mitogens, and cytokines and has been shown to induce inflammation-related diseases by facilitating the production of large amounts of prostaglandins. Thus, prostaglandins produced by COX-2 are thought to mediate the inflammatory response [20][21][22] . In this study, we showed that LPS significantly stimulated PGE 2 production and that the AKR-E effectively inhibited the production of PGE 2 in RAW 264.7 macrophages (Figure 3).…”

Section: Lps-induced Production Of No and Pge 2 Was Markedly Inhibitementioning

confidence: 99%

Acanthopanax koreanum roots inhibit the expression of pro-inflammatory cytokines, inducible nitric oxide synthase, and cyclooxygenase-2 in RAW 264.7 macrophages

Yang¹,

Hyun²,

Kim³

et al. 2016

Orient. J. Chem

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Acanthopanax koreanum is a popular plant found onJejuIsland, Korea and is commonly used to prevent the side effects of consumption of alcoholic beverages. However, this plant has not been properly utilized as a medicinal material. In this study, we investigated the anti-inflammatory effects of the 70% ethanol extract of A. koreanum roots (AKR-E). The results indicated that the AKR-E (200 µg/mL) inhibited the lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) in RAW 264.7 macrophages by 41.2% and 78.9%, respectively. These effects were accompanied by concentration-dependent decreases in the expression levels of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins. Additionally, the AKR-E inhibitedthe expression of pro-inflammatory cytokines, including interleukin (IL)-6 (22.7%) and IL-1β (74%). These data showed that the AKR-E had protective effects against the induction of LPS-induced inflammation in RAW 264.7 macrophages.

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Modulation of inducible nitric oxide synthase induction by prostaglandin E2 in macrophages: distinct susceptibility in murine J774 and RAW 264.7 macrophages☆

Cited by 27 publications

References 37 publications

Cross-Regulation of iNOS and COX-2 by its Products in Murine Macrophages Under Stress Conditions

Cross-Regulation of iNOS and COX-2 by its Products in Murine Macrophages Under Stress Conditions

Potentiation of Lipopolysaccharide-Induced IL-6 Release by Uridine Triphosphate in Macrophages: Cross-Interaction with Cyclooxygenase-2-Dependent Prostaglandin E<sub>2</sub> Production

Acanthopanax koreanum roots inhibit the expression of pro-inflammatory cytokines, inducible nitric oxide synthase, and cyclooxygenase-2 in RAW 264.7 macrophages

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