p38 Mitogen-activated Protein Kinase Down-regulates Nitric Oxide and Up-regulates Prostaglandin E2 Biosynthesis Stimulated by Interleukin-1β

Guan, Zhonghong; Baier, Lisa D.; Morrison, Adam

doi:10.1074/jbc.272.12.8083

Cited by 175 publications

(136 citation statements)

References 34 publications

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“…Similar ¢nd-ings have been reported for COX-2 induction in IL-1-stimulated mesangial cells [12] and LPS-stimulated monocytes [13].…”

Section: Introductionsupporting

confidence: 87%

“…4-(4-Fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridinyl) imidazole (SB 203580) was from Calbiochem. [Q-QP P]ATP (3000 Ci/mmol), [K-QP P]dCTP (3000 Ci/mmol), [K-QP P]UTP (800 Ci/mmol) and [ IR C]acetyl coenzyme A (55 Ci/mmol) were from Amersham Life, [5,6,7,8,11,12,14,15(N)-Q H]arachidonic acid (185 Ci/mmol) was from NEN.…”

Section: Methodsmentioning

confidence: 99%

“…IL-1 stimulation and other cell treatments were also under these conditions. [5,6,7,8,9,11,12,14,15-Q H(N)]arachidonic acid HeLa cells were grown to approximately 70% con£uence in 12-well (22 mm diameter) dishes. The medium was removed and replaced with 1 ml DMEM/10% (v/v) FCS containing 0.5 WCi [5,6,7,8,9,11,12,14,15-Q H](N)]arachidonic acid (184.6 Ci/mmol) per ml.…”

Section: Cell Culturementioning

confidence: 99%

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A p38 MAP kinase inhibitor regulates stability of interleukin‐1‐induced cyclooxygenase‐2 mRNA

Ridley¹,

Dean²,

Sarsfield³

et al. 1998

FEBS Letters

188

130

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The mechanism by which p38 mitogen-activated protein kinase (MAPK) regulates the induction of cyclooxygenase (COX)-2 by interleukin-1 (IL-1) has been investigated in HeLa cells. SB 203580, an inhibitor of p38 MAPK, in the range 0.1^1 W WM inhibited IL-1-stimulated PGE 2 (but not arachidonic acid) release and this was associated with inhibition of induction of COX-2 protein and mRNA. IL-1 stimulated COX-2 transcription in HeLa cells about 2-fold as judged by both reporter gene and nuclear run-on assays. The inhibitor had no significant effect on this. However, in cells previously stimulated with IL-1 it caused rapid destabilisation of COX-2 mRNA independently of on-going transcription. The results suggest a novel function for p38 MAPK in the regulation of mRNA stability.z 1998 Federation of European Biochemical Societies.

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“…Similar ¢nd-ings have been reported for COX-2 induction in IL-1-stimulated mesangial cells [12] and LPS-stimulated monocytes [13].…”

Section: Introductionsupporting

confidence: 87%

Section: Methodsmentioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

See 1 more Smart Citation

A p38 MAP kinase inhibitor regulates stability of interleukin‐1‐induced cyclooxygenase‐2 mRNA

Ridley¹,

Dean²,

Sarsfield³

et al. 1998

FEBS Letters

188

130

View full text Add to dashboard Cite

show abstract

“…Less information is available on the role of p38 as a regulator of endogenous genes in primary cells. In cell lines, TNF-induced IL-6 mRNA, stress-induced c-fos and c-jun mRNA, and IL-1-induced prostaglandin endoperoxide synthase-2 (PGHS-2) mRNA are suppressed by p38 inhibitors [17,19,[22][23][24][25]. More recently, suppression of PGHS-2 mRNA induction in primary monocytes was reported [26].…”

Section: Introductionmentioning

confidence: 99%

SB202190, a selective inhibitor of p38 mitogen-activated protein kinase, is a powerful regulator of LPS-induced mRNAs in monocytes

Manthey

Wang

Kinney

et al. 1998

Journal of Leukocyte Biology

163

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Inhibitors of p38 mitogen-activated protein kinase (p38) have been reported to block tumor necrosis factor ␣ (TNF-␣) and interleukin-1␤ (IL-1␤) production in monocytes at the level of mRNA translation. Yet, several studies document that p38 can phosphorylate and activate specific transcription factors. Thus, to understand better the role of p38 during monocyte activation, we sought to determine the extent to which p38 is required for lipopolysaccharide (

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“…IL-1 also activates MAP kinase pathways: p38 (Guan et al, 1997), ERK 1/2 ( (Laporte et al, 1999) and JNK (Guan et al, 1998) and subsequently activates transcription factors such as NF-kb (Roshak et al, 1996). In addition, modulation of IL-1R signalling is altered by other signalling proteins such as Smads, SOCSs (suppressor of cytokine signalling; Yoshimura et al, 2003) and STATs (Morton et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas

et al. 2005

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Ovulation is believed to contribute to the development of ovarian cancers that derive from the ovarian surface epithelium (OSE). The process of ovulation is synonymous with inflammation and inflammatory cytokines such as interleukin-1a (IL-1a) have recently been shown to induce both inflammatory and anti-inflammatory responses in human OSE (HOSE) cells. In this study we directly compared levels of IL-1a-induced gene expression by analysing the levels of 11b-hydroxysteroid dehydrogenase (11bHSD) types 1 (11bHSD-1) and 2 (11bHSD-2), cyclooxygenase-2 (COX-2), IL-1 receptor (IL-1R) and glucocorticoid receptor a (GRa) mRNA between normal HOSE cells and cell lines derived from poorly differentiated (SKOV-3, BG-1, PEO-4) and well-differentiated (PEO-14) ovarian adenocarcinoma. In HOSE cell cultures, and to a lesser extent PEO-14 cells, the basal mRNA levels of COX-2 and 11bHSD-1 were relatively high and further shown to be induced in response to IL-1a (for HOSE cells; 420-fold, Po0.05 and PEO-14 cells; 43fold, Po0.05). However, whereas HOSE cells expressed a low level of 11bHSD-2 mRNA that was only mildly responsive to IL-1a (1.3-fold, Po0.001), all cell lines exhibited a higher basal level of 11bHSD-2 mRNA that was in some cases further stimulated in PEO-4 cells (five-fold; Po0.05) or suppressed in SKOV-3 cells (two-fold; Po0.01) in response to IL-1a. All cells tested expressed IL-1R and, with the exception of BG-1, GRa. These results indicate that cell lines derived from ovarian cancers have lost the ability to respond normally to inflammatory cytokines such as IL-1a. The finding that normal OSE cells, in contrast to cell lines derived from patients with ovarian adenocarcinoma, abundantly express 11bHSD-1 mRNA but are essentially devoid of 11bHSD-2 mRNA supports the concept that the pattern of 11bHSD isoform gene expression is a defining feature of neoplastic cellular transformation, which might have particular relevance to the ovary.

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p38 Mitogen-activated Protein Kinase Down-regulates Nitric Oxide and Up-regulates Prostaglandin E2 Biosynthesis Stimulated by Interleukin-1β

Cited by 175 publications

References 34 publications

A p38 MAP kinase inhibitor regulates stability of interleukin‐1‐induced cyclooxygenase‐2 mRNA

A p38 MAP kinase inhibitor regulates stability of interleukin‐1‐induced cyclooxygenase‐2 mRNA

SB202190, a selective inhibitor of p38 mitogen-activated protein kinase, is a powerful regulator of LPS-induced mRNAs in monocytes

Inflammation-associated gene expression is altered between normal human ovarian surface epithelial cells and cell lines derived from ovarian adenocarcinomas

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