Regulation of BiP Gene Expression by Cyclopentenone Prostaglandins through Unfolded Protein Response Element

Odani, Noriko; Negishi, Manabu; Takahashi, Shouji; Kitano, Yoshimi; Kozutsumi, Yasunori; Ichikawa, Atsushi

doi:10.1074/jbc.271.28.16609

Cited by 27 publications

(29 citation statements)

References 24 publications

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“…Clearly, the exact mechanism of action of 15d-PGJ 2 in microglia remains undefined. One possible clue is the induction of heme oxygenase-1, BiP, and hsp70 by 15d-PGJ 2 as observed in other cell types (29,33,34). However, the doses of 15d-PGJ 2 used in those studies were about 10-fold higher than in this study, and it remains to be seen whether these effects are relevant to the inhibition of iNOS in microglia.…”

Section: Discussioncontrasting

confidence: 50%

Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ ^12,14 -prostaglandin J ₂

Petrova

Akama

Eldik

1999

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

305

229

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Mechanisms leading to down-regulation of activated microglia and astrocytes are poorly understood, in spite of the potentially detrimental role of activated glia in neurodegeneration. Prostaglandins, produced both by neurons and glia, may serve as mediators of glial and neuronal functions. We examined the inf luence of cyclopentenone prostaglandins and their precursors on activated glia. As models of glial activation, production of inducible nitric-oxide synthase (iNOS) was studied in lipopolysaccharide-stimulated rat microglia, a murine microglial cell line BV-2, and IL-1␤-stimulated rat astrocytes. Cyclopentenone prostaglandins were potent inhibitors of iNOS induction and were more effective than their precursors, prostaglandins E 2 and D 2 . 15-Deoxy-⌬ 12,14 -prostaglandin J 2 (15d-PGJ 2 ) was the most potent prostaglandin among those tested. In activated microglia, 15d-PGJ 2 suppressed iNOS promoter activity, iNOS mRNA, and protein levels. The action of 15d-PGJ 2 does not appear to involve its nuclear receptor peroxisome proliferator-activated receptor ␥ (PPAR␥) because troglitazone, a specific ligand of PPAR␥, was unable to inhibit iNOS induction, and neither troglitazone nor 15d-PGJ 2 could stimulate the activity of a PPAR-dependent promoter in the absence of cotransfected PPAR␥. 15d-PGJ 2 did not block nuclear translocation or DNA-binding activity of the transcription factor NFB, but it did inhibit the activity of an NFB reporter construct, suggesting that the mechanism of suppression of microglial iNOS by 15d-PGJ 2 may involve interference with NFB transcriptional activity in the nucleus. Thus, our data suggest the existence of a novel pathway mediated by cyclopentenone prostaglandins, which may represent part of a feedback mechanism leading to the cessation of inf lammatory glial responses in the brain.

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Section: Discussioncontrasting

confidence: 50%

Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ ^12,14 -prostaglandin J ₂

Petrova

Akama

Eldik

1999

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

305

229

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“…These findings support a PPAR␥-independent mechanism of UPR activation. PGJ 2 has been shown to localize to the ER, and this localization is associated with enhanced expression of GRP78 (BiP) and protein disulfide isomerase (43,44), suggesting that the actions of PGJ 2 are ER directed. Our findings suggest that PGJ 2 may exert effects directly or indirectly at the plasma membrane as the levels of cell death induced by PGJ 2 significantly differ depending on the biochemical assay being performed.…”

Section: Discussionmentioning

confidence: 99%

PGJ₂-stimulated β-cell apoptosis is associated with prolonged UPR activation

Chambers¹,

Weber²,

Corbett³

2007

American Journal of Physiology-Endocrinology and Metabolism

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“…Peroxisomal proliferator-activated receptor ␥ has been shown to be activated by PGJ 2 (75). PGJ 2 metabolites also activate the unfolded protein response element (76). We expect that other nuclear targets for other prostanoids will be identified.…”

Section: Minireview: Cyclooxygenases 33159mentioning

confidence: 99%

Prostaglandin Endoperoxide H Synthases (Cyclooxygenases)-1 and −2

Smith

Garavito

DeWitt

1996

Journal of Biological Chemistry

1,744

1,224

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Regulation of BiP Gene Expression by Cyclopentenone Prostaglandins through Unfolded Protein Response Element

Cited by 27 publications

References 24 publications

Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ ^12,14 -prostaglandin J ₂

Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ ^12,14 -prostaglandin J ₂

PGJ₂-stimulated β-cell apoptosis is associated with prolonged UPR activation

Prostaglandin Endoperoxide H Synthases (Cyclooxygenases)-1 and −2

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Regulation of BiP Gene Expression by Cyclopentenone Prostaglandins through Unfolded Protein Response Element

Cited by 27 publications

References 24 publications

Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ 12,14 -prostaglandin J 2

Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ 12,14 -prostaglandin J 2

PGJ2-stimulated β-cell apoptosis is associated with prolonged UPR activation

Prostaglandin Endoperoxide H Synthases (Cyclooxygenases)-1 and −2

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Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ ^12,14 -prostaglandin J ₂

Cyclopentenone prostaglandins suppress activation of microglia: Down-regulation of inducible nitric-oxide synthase by 15-deoxy-Δ ^12,14 -prostaglandin J ₂

PGJ₂-stimulated β-cell apoptosis is associated with prolonged UPR activation