Positive feedback regulation of COX-2 expression by prostaglandin metabolites

Vichai, Vanicha; Suyarnsesthakorn, C.; Pittayakhajonwut, D.; Sriklung, Kanlayanee; Kirtikara, Kanyawim

doi:10.1007/s00011-004-1338-1

Cited by 52 publications

(33 citation statements)

References 50 publications

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“…and PG production (67,68); however, the molecular mechanism for this phenomenon is not fully understood. Our data presented in this study reveal a novel cPLA 2 ␣-mediated PPAR␦ activation in PGE 2 -induced COX-2 expression in human cholangiocarcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

A Novel Positive Feedback Loop between Peroxisome Proliferator-activated Receptor-δ and Prostaglandin E2 Signaling Pathways for Human Cholangiocarcinoma Cell Growth

Han

2006

Journal of Biological Chemistry

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Peroxisome proliferator-activated receptor-␦ (PPAR␦) is a nuclear receptor implicated in lipid oxidation and the pathogenesis of obesity and diabetes. This study was designed to examine the potential effect of PPAR␦ on human cholangiocarcinoma cell growth and its mechanism of actions. Overexpression of PPAR␦ or activation of PPAR␦ by its pharmacological ligand, GW501516, at low doses (0.5-50 nM) promoted the growth of three human cholangiocarcinoma cell lines (CCLP1, HuCCT1, and SG231). This effect was mediated by

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Section: Discussionmentioning

confidence: 99%

A Novel Positive Feedback Loop between Peroxisome Proliferator-activated Receptor-δ and Prostaglandin E2 Signaling Pathways for Human Cholangiocarcinoma Cell Growth

Han

2006

Journal of Biological Chemistry

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“…Combining these results with the prevention of collagen deposition by the PAR-2 inhibitor sequence peptide strongly indicates that these tryptaseinduced changes in cardiac fibroblast phenotype utilize a PAR-2 dependent mechanism. Lastly, the use of PAR-2 antagonism led to a marked reduction in the amount of 15-d-PGJ 2 in the media which we originally hypothesized would be due to decreased COX-2 expression ( (Vichai et al 2005). Specifically, in that study only PGE 2 and 15-d-PGJ 2 were shown to induce COX-2 mRNA.…”

Section: Discussionmentioning

confidence: 94%

Tryptase activates isolated adult cardiac fibroblasts via protease activated receptor-2 (PAR-2)

Murray

McLarty-Williams

Nagalla

et al. 2011

J. Cell Commun. Signal.

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Protease activated receptor-2 (PAR-2) derived cycloxygenase-2 (COX-2) was recently implicated in a cardiac mast cell and fibroblast cross-talk signaling cascade mediating myocardial remodeling secondary to mechanical stress. We designed this study to investigate in vitro assays of isolated adult cardiac fibroblasts to determine whether binding of tryptase to the PAR-2 receptor on cardiac fibroblasts will lead to increased expression of COX-2 and subsequent formation of the arachodonic acid metabolite 15-dProstaglandin J 2 (15-d-PGJ 2 ). The effects of tryptase (100 mU) and co-incubation with PAR-2 inhibitor peptide sequence FSLLRY-NH 2 (10 -6 M) on proliferation, hydroxyproline concentration, 15-d-PGJ 2 formation and PAR-2/ COX-2 expression were investigated in fibroblasts isolated from 9 week old SD rats. Tryptase induced a significant increase in fibroproliferation, hydroxyproline, 15-d-PGJ 2 formation and PAR-2 expression which were markedly attenuated by FSLLRY. Tryptase-induced changes in cardiac fibroblast function utilize a PAR-2 dependent mechanism.

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“…Alternatively, it is also possible that the dramatic increase in COX-2 may be mediated, in part, through enhanced stabilization of COX-2 mRNA levels. Interestingly, PGE2 has a positive regulatory effect on COX-2 protein expression in mouse lung fibroblasts (40) and can stabilize COX-2 mRNA (41). The possibility that PGE2 stabilizes COX-2 mRNA stability and protein expression through a positive feedback mechanism in HLF after Ni and MALP-2 exposure is of interest and warrants further investigation.…”

Section: Discussionmentioning

confidence: 99%

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Brant¹,

Fabisiak²

2008

Am J Respir Cell Mol Biol

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Particulate matter air pollution (PM) has been linked with chronic respiratory diseases. Real-life exposures are likely to involve a mixture of chemical and microbial stimuli, yet little attention has been paid to the potential interactions between PM components (e.g., Ni) and microbial agents on the development of inflammatory-like conditions in the lung. Using the Toll-like receptor (TLR)-2 agonist MALP-2 as a lipopeptide relevant to microbial colonization, we hypothesized that nickel sensitizes human lung fibroblasts (HLF) for microbial-driven chemokine release through modulation of TLR signaling pathways. NiSO 4 (200 mM) synergistically enhanced CXCL8, yet antagonized CXCL10 mRNA expression and protein release from HLF in response to MALP-2. RT 2 -PCR pathway-focused array results indicated that NiSO 4 exposure did not alter the expression of TLRs or their downstream signaling mediators, yet significantly increased the expression of cyclooxygenase 2 (COX-2). Moreover, when NiSO 4 was given in combination with MALP-2, there was an amplified induction of COX-2 mRNA and protein along with its metabolic product, PGE2, in HLF. The COX-2 inhibitor, NS-398, attenuated NiSO 4 and MALP-2-induced PGE2 and CXCL8 release and partially reversed the NiSO 4 -dependent inhibition of MALP-2-induced CXCL10 release from HLF. These data indicate that NiSO 4 alters the pattern of TLR-2-dependent chemokine release from HLF via a COX-2-mediated pathway. The quantitative and qualitative effects of NiSO 4 on microbial-driven chemokine release from HLF shed new light on how PM-derived metals can exacerbate respiratory diseases.Keywords: COX-2; nickel; inflammation; chemokines; fibroblasts Particulate matter air pollution (PM) is a contributing risk factor for many adverse health effects, including respiratory diseases (1). Real-life scenarios are likely to involve exposures not only to chemical stresses such as PM, but microbial stimuli as well. While much attention has been paid to microbial-driven inflammation in the lung, limited information is available regarding the potential interactions between PM exposures and microbial stress on respiratory function. There are reports, however, of increased numbers of hospitalizations for respiratory disorders including infections on days of increased levels of PM (2). In support of these epidemiologic findings, several rodent models have shown PM exposure can increase susceptibility to infectious bacteria such as Listeria monocytogenes and Streptococcus pneumoniae (3, 4).Recent evidence suggests that colonization with species originally considered commensal and not causing overt disease (e.g., Mycoplasma fermentans) also has the potential to interact with other stimuli and/or alter biological responses in infected host cells (5, 6). For example, we have previously shown that exposure of human lung fibroblast cells (HLF) to M. fermentans synergistically enhances the release of IL-6 by PM in the form of residual oil fly ash (ROFA) compared to either stimulus alone (7). It is well recognized t...

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Positive feedback regulation of COX-2 expression by prostaglandin metabolites

Cited by 52 publications

References 50 publications

A Novel Positive Feedback Loop between Peroxisome Proliferator-activated Receptor-δ and Prostaglandin E2 Signaling Pathways for Human Cholangiocarcinoma Cell Growth

A Novel Positive Feedback Loop between Peroxisome Proliferator-activated Receptor-δ and Prostaglandin E2 Signaling Pathways for Human Cholangiocarcinoma Cell Growth

Tryptase activates isolated adult cardiac fibroblasts via protease activated receptor-2 (PAR-2)

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

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