MAP Kinase Pathways as a Route for Regulatory Mechanisms of IL-10 and IL-4 Which Inhibit COX-2 Expression in Human Monocytes

Niiro, Hiroaki; Otsuka, Takeshi; Ogami, Eiichi; Yamaoka, Kunihiro; Nagano, Shuji; Akahoshi, Mitsuteru; Nakashima, Hitoshi; Arinobu, Yojiro; Izuhara, Kenji; Niho, Yoshiyuki

doi:10.1006/bbrc.1998.9287

Cited by 96 publications

(56 citation statements)

References 27 publications

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“…IL-10 blocks activation of NF-B induced by lipopolysaccharide, TNF-␣, and reactive oxygen species (9,37). IL-10 also suppresses cyclooxgenase-2 expression by downregulation of p38 MAPK and ERK2 (31). Moreover, several reports have shown that IL-10 inhibits ERK1/2 activity and that this is important, for example, for the downregulation of polymorphonuclear neutrophil functions and CD40-mediated induction of IL-1␤ and TNF-␣ synthesis by monocytes (6,33,39).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-10 attenuates vascular responses to endothelin-1 via effects on ERK1/2-dependent pathway

Giachini¹,

Zemse²,

Carneiro³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Discussionmentioning

confidence: 99%

Interleukin-10 attenuates vascular responses to endothelin-1 via effects on ERK1/2-dependent pathway

Giachini¹,

Zemse²,

Carneiro³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…First, it has been reported that when anergy was induced in a T cell line, IL-10 production was increased, whereas JNK activity was blocked (42), suggesting a negative correlation between IL-10 and JNK activity, which is consistent with the present findings. Second, it has been shown that, in monocytes, IL-10 inhibited LPS-induced increase in activation of another mitogen-activated protein kinase, p38 (43). Third, IL-10 has been shown to inhibit the effect of TNF␣ in monocyte-derived dendritic cells, and this antagonism has been attributed to the ability of IL-10 to block the effect of TNF␣ on mitogen-activated protein kinases, including JNK (44).…”

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

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

127

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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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“…ERK1/2 is known to mediate the up-regulation of the inducible COX-2 in several mitogen-response assay systems, particularly in signaling pathways stimulated by interleukins and growth factors (Niiro et al, 1998;Sheng et al, 1998;Subbaramaiah et al, 1998;Zakar et al, 1998;Adderley and Fitzgerald, 1999;Barry et al, 1999). A relationship between ERK1/2 and COX-2 synthesis has not yet been suggested or examined with respect to cell-extracellular matrix substrate adhesion, however.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Cell-Substrate Adhesion by Arachidonic Acid: Lipoxygenase Regulates Cell Spreading and ERK1/2-inducible Cyclooxygenase Regulates Cell Migration in NIH-3T3 Fibroblasts

Stockton

Jacobson

2001

MBoC

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Adhesion of cells to an extracellular matrix is characterized by several discrete morphological and functional stages beginning with cell-substrate attachment, followed by cell spreading, migration, and immobilization. We find that although arachidonic acid release is rate-limiting in the overall process of adhesion, its oxidation by lipoxygenase and cyclooxygenases regulates, respectively, the cell spreading and cell migration stages. During the adhesion of NIH-3T3 cells to fibronectin, two functionally and kinetically distinct phases of arachidonic acid release take place. An initial transient arachidonate release occurs during cell attachment to fibronectin, and is sufficient to signal the cell spreading stage after its oxidation by 5-lipoxygenase to leukotrienes. A later sustained arachidonate release occurs during and after spreading, and signals the subsequent migration stage through its oxidation to prostaglandins by newly synthesized cyclooxygenase-2. In signaling migration, constitutively expressed cyclooxygenase-1 appears to contribute ϳ25% of prostaglandins synthesized compared with the inducible cyclooxygenase-2. Both the second sustained arachidonate release, and cyclooxygenase-2 protein induction and synthesis, appear to be regulated by the mitogen-activated protein kinase extracellular signal-regulated kinase (ERK)1/2. The initial cell attachment-induced transient arachidonic acid release that signals spreading through lipoxygenase oxidation is not sensitive to ERK1/2 inhibition by PD98059, whereas PD98059 produces both a reduction in the larger second arachidonate release and a blockade of induced cyclooxygenase-2 protein expression with concomitant reduction of prostaglandin synthesis. The second arachidonate release, and cyclooxygenase-2 expression and activity, both appear to be required for cell migration but not for the preceding stages of attachment and spreading. These data suggest a bifurcation in the arachidonic acid adhesion-signaling pathway, wherein lipoxygenase oxidation generates leukotriene metabolites regulating the spreading stage of cell adhesion, whereas ERK 1/2-induced cyclooxygenase synthesis results in oxidation of a later release, generating prostaglandin metabolites regulating the later migration stage. INTRODUCTIONCell adhesion to the extracellular matrix (ECM) is a sequential process of discrete temporal stages. Detached cells, e.g., leukocytes, metastasized cancer cells, or suspension-cultured cells, initially attach to an ECM protein substrate by means of plasma membrane receptors. Attached cells then undergo spreading, which results in flattening and the formation of focal adhesions. Subsequently, some cell types undergo migration on the ECM, whereas others remain stationary. Each of these stages of adhesion, i.e., attachment, spreading, migration, and immobilization, involves changes in morphology and cytoskeletal structure that are regulated by incompletely defined protein kinase and lipid second messenger pathways (reviewed in Huttenlocher et al., 1995;Heidemann an...

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MAP Kinase Pathways as a Route for Regulatory Mechanisms of IL-10 and IL-4 Which Inhibit COX-2 Expression in Human Monocytes

Cited by 96 publications

References 27 publications

Interleukin-10 attenuates vascular responses to endothelin-1 via effects on ERK1/2-dependent pathway

Interleukin-10 attenuates vascular responses to endothelin-1 via effects on ERK1/2-dependent pathway

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

Modulation of Cell-Substrate Adhesion by Arachidonic Acid: Lipoxygenase Regulates Cell Spreading and ERK1/2-inducible Cyclooxygenase Regulates Cell Migration in NIH-3T3 Fibroblasts

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