Interleukin 8-stimulated phosphatidylinositol-3-kinase activity regulates the migration of human neutrophils independent of extracellular signal-regulated kinase and p38 mitogen-activated protein kinases

Knall, Cindy; Worthen, G. Scott; Johnson, Gary L.

doi:10.1073/pnas.94.7.3052

Cited by 299 publications

(213 citation statements)

References 60 publications

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“…In contrast, the role of the MAPK pathways for chemotaxis is less clear, although its activation via chemokine receptors is well documented [33,[47][48][49]. One publication even showed that the MAPK pathways are dispensable for inducing a chemotactic response in human neutrophils [50]. In addition, it was shown that elevations of intracellular calcium are not necessary for directional migration of mouse neutrophils [36].…”

Section: Discussionmentioning

confidence: 99%

Vaccinia virus impairs directional migration and chemokine receptor switch of human dendritic cells

Humrich¹,

Thumann²,

Greiner³

et al. 2007

Eur J Immunol

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A crucial event for the induction of an anti-viral immune response is the coordinated, phenotype-dependent migration of dendritic cells (DC) to sites of infection and secondary lymphoid organs. Here we show that the vaccinia virus (VV) strains Western Reserve (WR) and modified virus Ankara (MVA) inhibit directional migration of mature DC toward the lymphoid chemokines CCL19 and CXCL12 without affecting surface expression of the respective chemokine receptors or impairing undirected cellular locomotion. Instead, infection with VV results in a deficiency of extracellular signalregulated kinase-1 and a disturbance of intracellular calcium mobilization, indicating a viral interference with signaling events downstream of the surface chemokine receptors. In immature DC, apart from inhibiting chemokine-induced migration of infected DC, infection with both VV strains increases expression of the inflammatory chemokine receptors CCR1 and CXCR1 on non-infected bystander DC, which depends on the activity of IFN-a. Although functional, these chemokine receptors are resistant to lipopolysaccharide-induced down-regulation. In addition, VV-infected and noninfected bystander DC fail to up-regulate the lymphoid chemokine receptor CCR7 upon activation, together pointing to a disability to undergo the chemokine receptor switch. This study shows that VV targets directional migration of professional antigenpresenting cells at multiple functional levels, revealing a potent viral strategy of immune escape.See accompanying commentary: http://dx

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Section: Discussionmentioning

confidence: 99%

Vaccinia virus impairs directional migration and chemokine receptor switch of human dendritic cells

Humrich¹,

Thumann²,

Greiner³

et al. 2007

Eur J Immunol

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“…9,10 One study showed that replacement of 2 tyrosine residues within the PI3K-binding sites of the PDGF ␤-receptor causes a loss of chemotactic response to PDGF-BB 21 ; however, another study demonstrated that PI3K inhibitors did not inhibit chemotaxis in SMCs and Swiss 3T3 cells. 22 In the present study, the inhibition of PI3K by wortmannin partially reduced PDGF-BB-induced SMC migration.…”

Section: Discussionmentioning

confidence: 99%

“…8 It has been previously reported that activation of the phosphatidylinositol 3Ј-kinase (PI3K) pathway is a rapid response to platelet-derived growth factor (PDGF), one of the most potent chemoattractants for SMCs, and is implicated in cellular motility, such as actin reorganization and membrane ruffling, in several cell types, including SMCs. 9,10 Moreover, it has been demonstrated recently that activation of mitogen-activated protein kinase (MAPK) pathways also plays a role in cell migration. Specifically, it has been reported that p38 MAPK , one of the MAPK pathways, may mediate the migratory action of tracheal SMCs in response to PDGF.…”

mentioning

confidence: 99%

Red Wine Polyphenols Inhibit Vascular Smooth Muscle Cell Migration Through Two Distinct Signaling Pathways

et al. 2002

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Background-Red wine polyphenols (RWPs) have been shown to have an antiatherogenic activity mainly through antioxidative effects on LDL oxidation. Although vascular smooth muscle cell (SMC) migration is critical to atherosclerosis formation, the effect of RWPs on SMC migration has not been elucidated. In this study, we investigated whether RWPs could affect the migration of cultured SMCs stimulated by growth factors. Methods and Results-RWP concentration dependently inhibited platelet-derived growth factor (PDGF)-BB-induced and serum-induced SMC migration in wounding assay and Boyden chamber assay. However, these inhibitory effects of RWPs were not seen in serum-stimulated vascular endothelial cell migration in either assay. Moreover, specific inhibitors of phosphatidylinositol-3Ј kinase (PI3K) and p38 mitogen-activated protein kinase (p38 MAPK ), but not of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), reduced PDGF-BB-induced SMC migration. To elucidate the signaling mechanism underlying the RWP effects, we investigated the effects of RWPs on the activity of PI3K and the phosphorylation of MAPK pathways in PDGF-BB-stimulated SMCs. RWPs inhibited the PI3K activity and p38MAPK phosphorylation, but not ERK1/2 phosphorylation, in a concentration-dependent manner. Moreover, the phosphorylation of MKK3/6, an upstream kinase of p38 MAPK , was also inhibited by RWP treatment in a concentrationdependent manner, suggesting that the inhibitory effect of RWPs on the p38 MAPK pathway works upstream of MKK3/6. The concentration-effect relationship of RWPs necessary for the inhibition of PI3K and p38MAPK pathways was similar to that of cell migration assays. Conclusions-RWPs inhibit the SMC migration through the inhibition of 2 distinct signaling pathways and thus exert antiatherogenic actions.

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“…In neutrophils, inhibiting the PI 3-kinase activity has been shown to decrease the downstream activation of the MAPK signaling cascade, e.g., activation of MEK, ERK, and MAPK [20,43,67]. In the study by Avdi and co-workers [43], the chemoattractant-induced activation of MEK kinase, MEK1, MEK2, as well as MAPK was shown to be inhibited by wortmannin while they proved to be independent of PI 3-kinase when activated by PMA.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of PI 3-kinase is an early event in neutrophil responses to chemoattractants and has been shown to participate in intracellular signaling, leading to processes such as chemotaxis, actin polymerization, degranulation, and adhesion [17,[19][20][21][22][23]. The PI 3-kinase is also involved in the signaling leading to NADPH-oxidase activation in response to formylmethionyl-leucyl-phenylalanine (fMLP [14,17,21,24]).…”

Section: Introductionmentioning

confidence: 99%

Phorbol myristate acetate induces neutrophil NADPH-oxidase activity by two separate signal transduction pathways: dependent or independent of phosphatidylinositol 3-kinase

Karlsson

Nixon

McPhail

2000

Journal of Leukocyte Biology

189

124

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The neutrophil NADPH-oxidase can be activated by protein kinase C (PKC) agonists such as phorbol myristate acetate (PMA), resulting in superoxide anion release. This superoxide release is independent of phosphatidylinositol 3-kinase (PI 3-kinase) because the inhibitor wortmannin does not affect the response. In this study, PMA is shown to also induce a wortmannin-sensitive NADPHoxidase activation, however, not resulting in release of superoxide but in intracellular production of the radical. This indicates that two pools of NADPH-oxidase, one localized in the plasma membrane and the other in the granule membranes, are separately regulated and the signal transduction pathways leading to activation of these pools differ regarding involvement of PI 3-kinase. Activation of both pools was dependent on ERK/MAPK kinase (MEK) activity and protein phosphatase 1 and/or 2A. As the two oxidase responses were differently affected by the inhibitor Gö -6850, different PKC isozymes are suggested to take part in the two signal transduction pathways. J. Leukoc. Biol. 67: 396-404; 2000.

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Interleukin 8-stimulated phosphatidylinositol-3-kinase activity regulates the migration of human neutrophils independent of extracellular signal-regulated kinase and p38 mitogen-activated protein kinases

Cited by 299 publications

References 60 publications

Vaccinia virus impairs directional migration and chemokine receptor switch of human dendritic cells

Vaccinia virus impairs directional migration and chemokine receptor switch of human dendritic cells

Red Wine Polyphenols Inhibit Vascular Smooth Muscle Cell Migration Through Two Distinct Signaling Pathways

Phorbol myristate acetate induces neutrophil NADPH-oxidase activity by two separate signal transduction pathways: dependent or independent of phosphatidylinositol 3-kinase

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