Interleukin 1 activates jun N‐terminal kinases JNK1 and JNK2 but not extracellular regulated MAP kinase (ERK) in human glomerular mesangial cells

Uciechowski, Peter; Saklatvala, Jeremy; Ohe, Juliane von der; Resch, Klaus; Szamel, Márta

doi:10.1016/0014-5793(96)00967-2

Cited by 34 publications

(27 citation statements)

References 21 publications

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“…In parallel, the stimulatory effect of IL-1␤ on JNK activation in hippocampal tissue was blocked by co-incubation in the presence of IL-10. We have reported previously (14,16) that IL-1␤ stimulated JNK activity in hippocampal tissue, supporting the findings of others (19) in a variety of different cell types. To our knowledge, this is the first report indicating that IL-10 suppresses the activation of JNK by IL-1␤ in brain tissue.…”

Section: Il-10 Antagonizes Il-1␤ Effect In Hippocampussupporting

confidence: 90%

“…However, IL-1␤ also inhibits transmitter release (6,7) and calcium channel activity (7,8) in the hippocampus, and it has been shown to inhibit long term potentiation (LTP) in CA1, CA3, and dentate gyrus in vitro (9 -11) and in dentate gyrus in vivo (12)(13)(14)(15); these effects are consistent with the high distribution of IL-1R1 in hippocampus (1)(2)(3)(4)(5). The inhibitory effects of IL-1␤ in hippocampus have been linked with stimulation of the stress-activated kinases, p38 and JNK (14,16), which have also been shown to be activated by IL-1␤ in other cells (17)(18)(19)(20). Evidence suggests that activation of IL-1 receptor-activated kinase (IRAK) is closely linked with JNK activation (21).…”

Section: Interleukin-1␤ (Il-1␤)mentioning

confidence: 99%

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The Anti-inflammatory Cytokine, Interleukin (IL)-10, Blocks the Inhibitory Effect of IL-1β on Long Term Potentiation

Kelly

Lynch

Vereker

et al. 2001

Journal of Biological Chemistry

125

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Several effects of the proinflammatory cytokine, interleukin-1␤ (IL-1␤), have been described in the central nervous system, and one area of the brain where marked changes have been reported is the hippocampus. Among these changes are an IL-1␤-induced inhibition of long term potentiation (LTP) in perforant path-granule cell synapses and an attenuation of glutamate release in synaptosomes prepared from the hippocampus. Evidence suggests that, at least in circulating cells, the anti-inflammatory cytokine, IL-10, antagonizes certain effects of IL-1. We investigated the effect of IL-10 on IL-1␤-induced inhibition of LTP and glutamate release. The evidence presented indicates that IL-1␤ stimulates the stress-activated protein kinase, c-Jun-activated protein kinase (JNK), and IL-1 receptor-associated kinase, which may explain its inhibitory effect on release and LTP, and that IL-10 reversed the IL-1␤-induced stimulation of JNK activity and inhibition of release and LTP. We observed that IL-10 abrogated the stimulatory effect of IL-1␤ on superoxide dismutase activity and reactive oxygen species production, whereas the H 2 O 2 -induced inhibition of LTP was also blocked by IL-10. We present evidence that suggests that the action of IL-10 may be mediated by its ability to induce shedding of the IL-1 type I receptor.

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Section: Il-10 Antagonizes Il-1␤ Effect In Hippocampussupporting

confidence: 90%

Section: Interleukin-1␤ (Il-1␤)mentioning

confidence: 99%

The Anti-inflammatory Cytokine, Interleukin (IL)-10, Blocks the Inhibitory Effect of IL-1β on Long Term Potentiation

Kelly

Lynch

Vereker

et al. 2001

Journal of Biological Chemistry

125

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“…Another difference between intestinal myofibroblasts and mesangial cells is that IL-1 has not been reported to activate ERKs in mesangial cells (55). ERK activation by IL-1 has recently been shown to depend on establishment of focal adhesions (30), and it is possible that, in the mesangial cell study mentioned, culture conditions were suboptimal for formation of focal adhesion complexes.…”

Section: Discussionmentioning

confidence: 99%

Regulation of COX-2 expression in human intestinal myofibroblasts: mechanisms of IL-1-mediated induction

Mifflin¹,

Saada²,

Mari³

et al. 2002

American Journal of Physiology-Cell Physiology

130

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Elevated mucosal interleukin-1 (IL-1) levels are frequently seen during acute and chronic intestinal inflammation, and IL-1 neutralization lessens the severity of inflammation. One major effect of IL-1 is the increased release of eicosanoid mediators via induction of cyclooxygenase-2 (COX-2). One site of COX-2-derived prostaglandin synthesis during acute and chronic intestinal inflammation is the intestinal myofibroblast. COX-2 expression has also been documented in these cells in colonic neoplasms. Thus an understanding of the regulation of COX-2 expression in human intestinal myofibroblasts is important. As an initial step toward this goal we have characterized IL-1α signaling pathways that induce COX-2 expression in cultured human intestinal myofibroblasts. IL-1 treatment resulted in a dramatic transcriptional induction of COX-2 gene expression. Activation of nuclear factor-κB (NF-κB), extracellular signal-regulated protein kinase (ERK), p38, and protein kinase C (PKC) signaling pathways was each necessary for optimal COX-2 induction. In contrast to what occurs in other cell types, including other myofibroblasts such as renal mesangial cells, PKC inhibition did not prevent IL-1-induced NF-κB or mitogen activated protein kinase/ stress-activated protein kinase activation, suggesting a novel role for PKC isoforms during this process. The stimulatory effects of PKC, NF-κB, ERK-1/2, and presumably c-Jun NH2-terminal kinase activation were exerted at the transcriptional level, whereas p38 activation resulted in increased stability of the COX-2 message. We conclude that, in intestinal myofibroblasts, IL-1-mediated induction of COX-2 expression is a complex process that requires input from multiple signaling pathways. Each parallel pathway acts in relative autonomy, the sum of their actions culminating in a dramatic increase in COX-2 transcription and message stability.

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“…Notably both IL-1␤ (49) and PAF (unpublished observations) but not IL-6 (49) activate the Jun N-terminal kinase JNK1 required for enhancement of AP1 transcriptional activation. Other cis-acting elements, including the Zn 2ϩ -containing DNA binding protein Egr1 (29), NF-B, which pre-exists as a latent dimeric activator in the cytoplasm (18,32), and the SIE and GAS factors, induced by interferons ␣ and ␥, respectively (9,37), have been shown to enhance basal transcription rates depending on their frequency and position relative to the core promoter (10,35).…”

Section: Fig 2 Paf or Il-1␤mentioning

confidence: 94%

Budesonide epimer R or dexamethasone selectively inhibit platelet-activating factor-induced or interleukin 1β-induced DNA binding activity ofcis-acting transcription factors and cyclooxygenase-2 gene expression in human epidermal keratinocytes

Lukiw¹,

Peláez²,

Martínez³

et al. 1998

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

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To further understand the molecular mechanism of glucocorticoid action on gene expression, DNA-binding activities of the cis-acting transcription factors activator protein 1 (AP1), AP2, Egr1 (zif268), NF-B, the signal transducers and activators of transcription proteins gamma interferon activation site (GAS), Sis-inducible element, and the TATA binding protein transcription factor II D (TFIID) were examined in human epidermal keratinocytes. The cytokine interleukin 1␤ (IL-1␤) and platelet-activating factor (PAF), both potent mediators of inflammation, were used as triggers for gene expression. Budesonide epimer R (BUDeR) and dexamethasone (DEX) were studied as potential antagonists. BUDeR or DEX before IL-1␤-or PAF-mediated gene induction elicited strong inhibition of AP1-, GAS-, and in particular NF-B-DNA binding (P < 0.001, ANOVA). Only small effects were noted on AP2, Egr1 (zif268), and Sis-inducible element-DNA binding (P > 0.05). No significant effect was noted on the basal transcription factor TFIID recognition of TATA-containing core promoter sequences (P > 0.68). To test the hypothesis that changing cis-acting transcription factor binding activity may be involved in inflammatoryresponse related gene transcription, RNA message abundance for human cyclooxygenase (COX)-1 and -2 (E.C.1.14.99.1) was assessed in parallel by using reverse transcription-PCR. Although the COX-1 gene was found to be expressed at constitutively low levels, the TATA-containing COX-2 gene, which contains AP1-like, GAS, and NF-B DNA-binding sites in its immediate promoter, was found to be strongly induced by IL-1␤ or PAF (P < 0.001). BUDeR and DEX both suppressed COX-2 RNA message generation; however, no correlation was associated with TFIID-DNA binding. These results suggest that on stimulation by mediators of inflammation, although the basal transcription machinery remains intact, modulation of cis-activating transcription factor AP1, GAS, and NF-B-DNA binding by the glucocorticoids BUDeR and DEX play important regulatory roles in the extent of specific promoter activation and hence the expression of key genes involved in the inflammatory response.Glucocorticosteroids (GCs) have long been used therapeutically as immunosuppressive and anti-inflammatory agents; however, the mechanism of their activity is only recently becoming understood at the genetic level. GCs interact with an intracellular GC receptor, which subsequently translocates to the nucleus as a ligand-activated transcriptional modulator. In turn, the GC receptor regulates the expression of genes such as those encoding cytokines, matrix metalloproteinases, and cell adhesion molecules known to be critical to both inflammation and the immune response (1, 2). Besides a direct "type 1" interaction with a palindromic GC responsive element in GC-sensitive gene promoters (3, 4), functions of the GC receptor also include a "type 2" interaction with chromatin-associated cis-acting transcription factors. For example, the GC receptor can physically interact with the Fos and J...

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Interleukin 1 activates jun N‐terminal kinases JNK1 and JNK2 but not extracellular regulated MAP kinase (ERK) in human glomerular mesangial cells

Cited by 34 publications

References 21 publications

The Anti-inflammatory Cytokine, Interleukin (IL)-10, Blocks the Inhibitory Effect of IL-1β on Long Term Potentiation

The Anti-inflammatory Cytokine, Interleukin (IL)-10, Blocks the Inhibitory Effect of IL-1β on Long Term Potentiation

Regulation of COX-2 expression in human intestinal myofibroblasts: mechanisms of IL-1-mediated induction

Budesonide epimer R or dexamethasone selectively inhibit platelet-activating factor-induced or interleukin 1β-induced DNA binding activity ofcis-acting transcription factors and cyclooxygenase-2 gene expression in human epidermal keratinocytes

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