Regulation of lysophosphatidic acid-induced COX-2 expression by ERK1/2 activation in cultured feline esophageal epithelial Cells

Kim, Do Young; Song, Hyun Ju; Jeong, Ji Hoon; Suh, Jung Sook; Sohn, Uy Dong

doi:10.1007/s12272-001-2114-1

Cited by 5 publications

(3 citation statements)

References 56 publications

(63 reference statements)

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“…Novel mechanisms for OxPC effects are likely, because even though COX2 and oxylipins are induced, pro-inflammatory mediators such as IL-1β or TNF that are typically associated with COX2 [67,68] are not. We show that OxPC activation of PKC is needed to induce COX2, and this is consistent with responses to other stimuli [69,70]. We also show that inhibiting COX2 activity or E1/E2 receptor-mediated response to COX2 metabolites blocks GM-CSF, but not IL-6 or IL-8 biosynthesis, whereas PKC inhibition effectively prevents release of all three cytokines.…”

Section: Discussionsupporting

confidence: 84%

Allergen inhalation generates pro-inflammatory oxidised phosphatidylcholine associated with airway dysfunction

et al. 2020

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RationaleOxidised phosphatidylcholines (OxPC) are produced under conditions of elevated oxidative stress and can contribute to human disease pathobiology. However, their role in allergic asthma is unexplored.ObjectivesCharacterise the OxPC profile in the airways after allergen challenge of people with airway hyperresponsiveness (AHR) or mild-asthma. Determine the capacity of OxPC to contribute to pathobiology associated with asthma.MethodsUsing bronchoalveolar lavage (BAL) from two human cohorts, OxPC species were quantified using ultra high performance liquid chromatography tandem mass spectrometry. Murine thin cut lung slices (TCLS) were used to measure airway narrowing caused by OxPCs. Human airway smooth muscle (HASM) cells were exposed to OxPCs to assess concentration-associated changes in inflammatory phenotype and activation of signalling networks.Measurements and Main ResultsOxPC profiles were different in the airways of people with or without AHR and correlated with methacholine responsiveness. Exposure of mild-asthmatics to allergens produced unique OxPC signatures that were associated with the late asthma response severity. OxPCs dose-dependently induced 15% airway narrowing in murine TCLS. In HASM, OxPCs dose-dependently increased the biosynthesis of cyclooxygenase-2, IL-6, IL-8, GM-CSF, and the production of oxylipins via protein kinase C-dependent pathways.ConclusionsData from human cohorts and primary HASM culture we show that OxPCs are present in the airways, increase after allergen challenge, and correlate with metrics of a dysfunction. Furthermore, OxPCs may contribute to asthma pathobiology by promoting airway narrowing and inducing a pro-inflammatory phenotype and contraction of airway smooth muscle. OxPCs represent a potential novel target for treating oxidative stress-associated pathobiology in asthma.

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Section: Discussionsupporting

confidence: 84%

Allergen inhalation generates pro-inflammatory oxidised phosphatidylcholine associated with airway dysfunction

et al. 2020

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“…The sliced tissue was placed into DMEM supplemented with 10% FBS containing 100 U/ml penicillin, 0.1 mg/ml streptomycin, and 0.25 µg/ml amphotericin B and incubated in a humidified atmosphere of 5% CO 2 and 95% air at 37℃ [31]. After 10 days, the medium was exchanged with fresh DMEM containing 10% FBS.…”

Section: Methodsmentioning

confidence: 99%

The Protective Effect of Eupatilin against Hydrogen Peroxide-Induced Injury Involving 5-Lipoxygenase in Feline Esophageal Epithelial Cells

Lim

Park

Nam

et al. 2012

Korean J Physiol Pharmacol

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In this study, we focused to identify whether eupatilin (5,7-dihydroxy-3',4',6-trimethoxyflavone), an extract from Artemisia argyi folium, prevents H2O2-induced injury of cultured feline esophageal epithelial cells. Cell viability was measured by the conventional MTT reduction assay. Western blot analysis was performed to investigate the expression of 5-lipoxygenase by H2O2 treatment in the absence and presence of inhibitors. When cells were exposed to 600 µM H2O2 for 24 hours, cell viability was decreased to 40%. However, when cells were pretreated with 25~150 µM eupatilin for 12 hours, viability was significantly restored in a concentration-dependent manner. H2O2-treated cells were shown to express 5-lipoxygenase, whereas the cells pretreated with eupatilin exhibited reduction in the expression of 5-lipoxygenase. The H2O2-induced increase of 5-lipoxygenase expression was prevented by SB202190, SP600125, or NAC. We further demonstrated that the level of leukotriene B4 (LTB4) was also reduced by eupatilin, SB202190, SP600125, NAC, or nordihydroguaiaretic acid (a lipoxygenase inhibitor) pretreatment. H2O2 induced the activation of p38MAPK and JNK, this activation was inhibited by eupatilin. These results indicate that eupatilin may reduce H2O2-induced cytotoxicity, and 5-lipoxygenase expression and LTB4 production by controlling the p38 MAPK and JNK signaling pathways through antioxidative action in feline esophageal epithelial cells.

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“…However, the signal transduction pathways leading to sPLA 2 MT-III-promoted protein expression of COX-2 and production of AA and PGE 2 levels in macrophages are still poorly understood. It is known that membrane cleavage products generated by sPLA 2 s are important bioactive mediators involved in the induction and release of COX-2 and PGE 2 , respectively, by activating intracellular signaling mechanisms in various cells (Ruipérez et al, 2007;Kim et al, 2008;Hughes-Fulford et al, 2001;Oh detal., 2000 ).…”

Section: Introductionmentioning

confidence: 99%

12-HETE is a regulator of PGE2 production via COX-2 expression induced by a snake venom group IIA phospholipase A2 in isolated peritoneal macrophages

Moreira

Gutiérrez

Lomonte

et al. 2020

Chemico-Biological Interactions

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The inducible cyclooxygenase (COX)-2 and prostaglandin (PG)E 2 production are distinctly regulated by several kinase pathways, most of which mediated by the NF-κB activation, in peritoneal macrophages stimulated by the snake venom secreted phospholipase A 2 (sPLA 2) myotoxin (MT)-III. However, the mechanism by which this group IIA sPLA 2 exerts its inflammatory effect on macrophages is not fully understood. Increasing evidence suggest that 12-HETE, a product from arachidonic acid metabolism by 12-LO activation, is implicated in amplifying inflammation by regulating cell functions. In the present study the crosswise link between 12-HETE and MT-III-induced COX-2 and PGE 2 release, associated to signaling pathways mediated by p38MAPK, PKC, ERK and NF-κB, were investigated. Results demonstrated that stimulation of isolated macrophages with MT-III cause activation of 12-LO in a time-dependent manner, with significant release of 12-HETE and without modification of 12-LO protein levels. The involvement of 12-HETE in MT-III-induced COX-2 expression and PGE 2 production was demonstrated by using the selective 12-LO inhibitor baicalein. A significant decrease in the phosphorylation levels of MT-III-induced ERK1/2, but not of p38MAPK nor PKC, was observed in macrophages pre-incubated with the 12-LO inhibitor. In turn, MT-III-induced COX-2 protein expression and PGE 2 release, but not NF-κB activation, were attenuated by pre-treating cells with PD98059, indicating the involvement of distinct pathways mediated by ERK in isolated macrophages. These results suggest that, in macrophages, MT-III-induced COX-2 protein expression and PGE 2 release are distinctly and sequentially mediated through 12-HETE followed by ERK pathway activation, but are independent on NF-κB activation. Taken together, our findings highlight an unprecedented mechanism by which 12-HETE regulates one of the distinct signaling pathways for MT-III-induced COX-2 expression and PGE 2 release in macrophages. These results provide new knowledge on the proinflammatory mechanisms of action of group IIA sPLA 2 from snake venom.

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Regulation of lysophosphatidic acid-induced COX-2 expression by ERK1/2 activation in cultured feline esophageal epithelial Cells

Cited by 5 publications

References 56 publications

Allergen inhalation generates pro-inflammatory oxidised phosphatidylcholine associated with airway dysfunction

Allergen inhalation generates pro-inflammatory oxidised phosphatidylcholine associated with airway dysfunction

The Protective Effect of Eupatilin against Hydrogen Peroxide-Induced Injury Involving 5-Lipoxygenase in Feline Esophageal Epithelial Cells

12-HETE is a regulator of PGE2 production via COX-2 expression induced by a snake venom group IIA phospholipase A2 in isolated peritoneal macrophages

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