Differential mRNA expression of prostaglandin receptor subtypes in macrophage activation

Hubbard, Neil E.; Lee, Seung‐Hyo; Lim, Debora; Erickson, Kent L.

doi:10.1054/plef.2001.0327

Cited by 38 publications

(32 citation statements)

References 26 publications

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“…4). The inability of PGE 2 to elevate IP 3 or Ca 2ϩ levels is consistent with reports that RAW264.7 cells lack the calcium-coupled EP 1 and EP 3 receptors (12)(13)(14). The lack of an effect with thapsigargin is consistent with reports that it increases cytosolic Ca 2ϩ levels in a phospholipase C-and IP 3 -independent fashion, primarily by inhibiting SERCA (sarcoendoplasmic reticulum Ca 2ϩ re-uptake) pumps (18,19).…”

Section: Pge2-g Induces Increases In Ip3 Levels In Raw2647 Cellssupporting

confidence: 88%

The glyceryl ester of prostaglandin E₂mobilizes calcium and activates signal transduction in RAW264.7 cells

Nirodi

Crews

Kozak

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

108

107

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Glyceryl prostaglandins (PG-Gs) are generated by the oxygenation of the endocannabinoid, 2-arachidonylglycerol, by cyclooxygenase 2. The biological consequences of this selective oxygenation are uncertain because the cellular activities of PG-Gs have yet to be defined. We report that the glyceryl ester of PGE 2, PGE2-G, triggers rapid, concentration-dependent Ca 2؉ accumulation in a murine macrophage-like cell line, RAW264.7. Ca 2؉ mobilization is not observed after addition of PGE 2, PGD2-G, or PGF2␣-G but is observed after addition of PGF 2␣. Moreover, PGE2-G, but not PGE2, stimulates a rapid but transient increase in the levels of inositol 1,4,5-trisphosphate (IP 3) as well as the membrane association and activation of PKC. PGE 2-G induces a concentration-dependent increase in the levels of phosphorylated extracellular signal regulated kinases 1 and 2 through a pathway that requires the activities of PKC, IP 3 receptor, and phospholipase C ␤. The results indicate that PGE2-G triggers Ca 2؉ mobilization, IP3 synthesis, and activation of PKC in RAW264.7 macrophage cells at low concentrations. These responses are independent of the hydrolysis of PGE 2-G to PGE2.

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Section: Pge2-g Induces Increases In Ip3 Levels In Raw2647 Cellssupporting

confidence: 88%

The glyceryl ester of prostaglandin E₂mobilizes calcium and activates signal transduction in RAW264.7 cells

Nirodi

Crews

Kozak

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

108

107

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“…It is possible that increased PGE 2 production by lung fibroblasts following fibrotic challenge may contribute to the down-regulation of the EP2 receptor. Previous studies have demonstrated that treatment of macrophages with exogenous PGE 2 can inhibit both EP2 and EP4 expression (37). We have observed that the fibroblasts isolated postbleomycin in the present studies do in fact secrete elevated levels of PGE 2 at days 14 and 21 postbleomycin (approximately a 65% increase at both time points compared with day 0; data not shown).…”

Section: Discussionsupporting

confidence: 69%

“…In macrophages, LPS has been reported to increase levels of EP2 (37,39). EP4 receptors have been reported to be both elevated (38) and reduced by LPS treatment (39).…”

Section: Discussionmentioning

confidence: 99%

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Bleomycin-Induced E Prostanoid Receptor Changes Alter Fibroblast Responses to Prostaglandin E2

Moore

Ballinger

White

et al. 2005

The Journal of Immunology

125

109

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Although PGE2 is a potent inhibitor of fibroblast function, PGE2 levels are paradoxically elevated in murine lungs undergoing fibrotic responses. Pulmonary fibroblasts from untreated mice expressed all four E prostanoid (EP) receptors for PGE2. However, following challenge with the fibrogenic agent, bleomycin, fibroblasts showed loss of EP2 expression. Lack of EP2 expression correlated with an inability of fibroblasts from bleomycin-treated mice to be inhibited by PGE2 in assays of proliferation or collagen synthesis and blunted cAMP elevations in response to PGE2. PGE2 was similarly unable to suppress proliferation or collagen synthesis in fibroblasts from EP2−/− mice despite expression of the other EP receptors. EP2−/−, but not EP1−/− or EP3−/− mice, showed exaggerated fibrotic responses to bleomycin administration in vivo as compared with wild-type controls. EP2 loss on fibroblasts was verified in a second model of pulmonary fibrosis using FITC. Our results for the first time link EP2 receptor loss on fibroblasts following fibrotic lung injury to altered suppression by PGE2 and thus identify a novel fibrogenic mechanism.

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“…Although we did not determine the protein expression levels of each EP-receptor subtype, the present mRNA data suggest that nephritic glomeruli would express less EP receptors than normal glomeruli. Hubbard et al demonstrated prostaglandin E 2 -and dibutyryl cyclic AMP-induced diminution of expression levels of EP 2 and EP 4 receptors using RAW 264.7 cells (22). The nephritic glomeruli generate more prostaglandin E 2 than the normal glomeruli (Fig.…”

Section: Discussionmentioning

confidence: 94%

Protective Effect of Prostaglandin EP4-Receptor Agonist on Anti-glomerular Basement Membrane Antibody-Associated Nephritis

et al. 2006

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Abstract. Prostaglandin E 2 -receptor subtypes, EP 1 , EP 2 , EP 3 , and EP 4 , are present in the kidney. The aim of this study was to elucidate the anti-nephritic effect of an EP 4 -receptor agonist on an experimental nephritic model. Mice were injected i.v. with anti-glomerulus antiserum to induce nephritis. Nephritic glomeruli generated more prostaglandin E 2 (2.6 and 0.7 ng) and less cyclic AMP than normal glomeruli (11 and 26 pmol). The production of cyclic AMP in nephritic glomeruli increased 67% in response to AE1-329, an EP 4 agonist, at 10 −5 M. Nephritic glomeruli expressed a lesser amount of mRNA of prostaglandin E 2 -receptor subtypes as compared with normal glomeruli. AE1-329 was administered s.c. at 100 µg/ kg per day for 3 weeks. AE1-329 suppressed the increase in creatinine and cholesterol compared to those in the control nephritic mice. AE1-329-treated nephritic mice had less crescentic glomeruli and less deposition of rabbit IgG (anti-glomerular basement membrane antibody) in glomeruli than the control mice. AE1-329 prevented the development of glomerulonephritis. These findings suggest that EP 4 -receptor agonists are a promising drug to prevent the development of glomerulonephritis.

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Differential mRNA expression of prostaglandin receptor subtypes in macrophage activation

Cited by 38 publications

References 26 publications

The glyceryl ester of prostaglandin E₂mobilizes calcium and activates signal transduction in RAW264.7 cells

The glyceryl ester of prostaglandin E₂mobilizes calcium and activates signal transduction in RAW264.7 cells

Bleomycin-Induced E Prostanoid Receptor Changes Alter Fibroblast Responses to Prostaglandin E2

Protective Effect of Prostaglandin EP4-Receptor Agonist on Anti-glomerular Basement Membrane Antibody-Associated Nephritis

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Differential mRNA expression of prostaglandin receptor subtypes in macrophage activation

Cited by 38 publications

References 26 publications

The glyceryl ester of prostaglandin E2mobilizes calcium and activates signal transduction in RAW264.7 cells

The glyceryl ester of prostaglandin E2mobilizes calcium and activates signal transduction in RAW264.7 cells

Bleomycin-Induced E Prostanoid Receptor Changes Alter Fibroblast Responses to Prostaglandin E2

Protective Effect of Prostaglandin EP4-Receptor Agonist on Anti-glomerular Basement Membrane Antibody-Associated Nephritis

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The glyceryl ester of prostaglandin E₂mobilizes calcium and activates signal transduction in RAW264.7 cells

The glyceryl ester of prostaglandin E₂mobilizes calcium and activates signal transduction in RAW264.7 cells