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231222s2001 xx ||||| 00| ||eng c |
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|a pubmed24n1460.xml
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|a (DE-627)NLM111487986
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|a (NLM)11237557
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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100 |
1 |
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|a Reilly, C M
|e verfasserin
|4 aut
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1 |
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|a Prostaglandin J(2) inhibition of mesangial cell iNOS expression
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|c 2001
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336 |
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|a Text
|b txt
|2 rdacontent
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337 |
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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|a Band
|b nc
|2 rdacarrier
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|a Date Completed 29.03.2001
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|a Date Revised 04.07.2024
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|a published: Print
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|a Citation Status MEDLINE
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|a Copyright 2001 Academic Press.
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|a Mesangial cells from MRL/lpr mice, a model of lupus, overproduce nitric oxide (NO) compared to controls. J series prostaglandins (PG) and thiazolidinediones block LPS stimulation of NO production via the activation of peroxisome proliferator-activator receptor-gamma (PPAR-gamma) in macrophages but utilize an alternative mechanism in microglial cells. We investigated the mechanism by which PGJ(2) inhibits NO production in LPS/IFN-gamma-stimulated MRL/lpr mesangial cells. Our results demonstrated that LPS/IFN-gamma addition to MRL/lpr mesangial cells stimulated iNOS activation, expression of p-38 kinase and p44/42 MAPK, and NF-kappaB translocation to the nucleus. Both pioglitazone, a specific PPAR-gamma agonist, and PGJ(2) blocked NO production, iNOS protein expression, and iNOS mRNA transcription. PGJ(2) failed to inhibit nuclear NF-kappaB translocation or p44/42 MAPK or p-38 kinase induction in stimulated mesangial cells. These data suggest that PGJ(2) blocks iNOS expression and subsequent NO production in mesangial cells via a PPAR-gamma-mediated mechanism either by interfering with NF-kappaB transcriptional activity or by an NF-kappaB-independent mechanism
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Research Support, U.S. Gov't, P.H.S.
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|a Lipopolysaccharides
|2 NLM
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|a NF-kappa B
|2 NLM
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|a Receptors, Cytoplasmic and Nuclear
|2 NLM
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|a Transcription Factors
|2 NLM
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|a 9-deoxy-delta-9-prostaglandin D2
|2 NLM
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|a 60203-57-8
|2 NLM
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|a Interferon-gamma
|2 NLM
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|a 82115-62-6
|2 NLM
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|a Nitric Oxide Synthase
|2 NLM
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|a EC 1.14.13.39
|2 NLM
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|a Nitric Oxide Synthase Type II
|2 NLM
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|a EC 1.14.13.39
|2 NLM
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|a Nos2 protein, mouse
|2 NLM
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|a EC 1.14.13.39
|2 NLM
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|a Mitogen-Activated Protein Kinases
|2 NLM
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|a EC 2.7.11.24
|2 NLM
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|a Prostaglandin D2
|2 NLM
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|a RXY07S6CZ2
|2 NLM
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1 |
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|a Oates, J C
|e verfasserin
|4 aut
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1 |
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|a Sudian, J
|e verfasserin
|4 aut
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1 |
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|a Crosby, M B
|e verfasserin
|4 aut
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1 |
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|a Halushka, P V
|e verfasserin
|4 aut
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1 |
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|a Gilkeson, G S
|e verfasserin
|4 aut
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773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 98(2001), 3 vom: März, Seite 337-45
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
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|g volume:98
|g year:2001
|g number:3
|g month:03
|g pages:337-45
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_350
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|a AR
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|d 98
|j 2001
|e 3
|c 03
|h 337-45
|