Common and distinct intracellular signaling pathways in human neutrophils utilized by platelet activating factor and FMLP.

Nick, Jerry A.; Avdi, Natalie J.; Young, Shamar; Knall, Cindy; Gerwins, Pär; Johnson, Gary L.; Worthen, G. Scott

doi:10.1172/jci119263

Cited by 292 publications

(297 citation statements)

References 56 publications

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“…Preincubation of rat neutrophils with pertussis toxin (PTX), a potent endotoxin that catalyzes ADP-ribosylation of G iao , greatly inhibited ERK activation by fMLP (Fig. 1), consistent with the previous reports in human neutrophils [11,14].…”

Section: Phosphorylation Of Erk Via a G Protein-dependent Andsupporting

confidence: 90%

“…However, the signal transduction events upstream to ERK occurring in neutrophils in response to fMLP have been incompletely delineated. Based on immunoblot analysis with anti-phosphop44/42 MAPK antibodies, we found that exposure of neutrophils to fMLP rapidly induced the activation of ERK, reconcile the earlier reports [14,15], and these responses were attenuated by 0.3 WM U0126 ( Fig. 1) as well as 3 WM PD98059 (data not shown), both selective MEK inhibitors [16,17].…”

Section: Phosphorylation Of Erk Via a G Protein-dependent Andsupporting

confidence: 89%

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Examination of the signal transduction pathways leading to activation of extracellular signal‐regulated kinase by formyl‐methionyl‐leucyl‐phenylalanine in rat neutrophils

Chang

Wang

1999

FEBS Letters

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The signaling pathways leading to extracellular signal-regulated kinase (ERK) activation in formyl-methionylleucyl-phenylalanine (fMLP)-stimulated rat neutrophils were examined. fMLP-stimulated ERK activation based on immunoblot analysis with antibodies against the phosphorylation form of ERK was attenuated by the pretreatment of cells with pertussis toxin but not with a dual cyclo-oxygenase/lipoxygenase inhibitor BW755C. Exposure of cells to the tyrosine kinase inhibitor genistein, phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002, or protein kinase C (PKC) inhibitors Go «6976, Go «6983, and GF109203X inhibited fMLP-stimulated ERK phosphorylation in a concentration-dependent manner. In addition, both the phospholipase C (PLC) inhibitor U73122 and the Ca 2 chelator BAPTA attenuated ERK activation. These results indicate that G iao protein, tyrosine kinase, PI3K, PKC, and PLC/Ca 2 , but not arachidonate metabolites, act upstream of fMLP-stimulated ERK activation.z 1999 Federation of European Biochemical Societies.

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Section: Phosphorylation Of Erk Via a G Protein-dependent Andsupporting

confidence: 90%

Section: Phosphorylation Of Erk Via a G Protein-dependent Andsupporting

confidence: 89%

Examination of the signal transduction pathways leading to activation of extracellular signal‐regulated kinase by formyl‐methionyl‐leucyl‐phenylalanine in rat neutrophils

Chang

Wang

1999

FEBS Letters

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“…From the pharmacological experiments, we propose that PAF induces chemotaxis via a Gi-dependent and MAPK-dependent pathway in rat microglia. Little is known regarding the molecular mechanisms underlying chemotaxis; p38 MAPK is responsible for PAF-induced neutrophil movement (Nick et al 1997), whereas Erk1/2 activation in¯uences ®broblastic cell migration (Klemke et al 1997). Further investigations are necessary to identify subsequent signals that link the activation of MAPK to chemotaxis.…”

Section: Activation Of Gi and Mapk Is Required For Chemotaxis Of Micrmentioning

confidence: 99%

Interaction between neurone and microglia mediated by platelet‐activating factor

et al. 2000

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“…13 Both PAF and fMLP are chemoattractants that bind to the neutrophil cell surface via members of the membrane-spanning GTP-binding protein (G protein) linked receptor family. [12][13][14] Platelet activating factor and fMLP have common and distinct signalling pathways in neutrophils. 14 The main common pathways are as follows.…”

Section: Discussionmentioning

confidence: 99%

“…[12][13][14] Platelet activating factor and fMLP have common and distinct signalling pathways in neutrophils. 14 The main common pathways are as follows. 15 The binding of either PAF or fMLP to its receptor in the neutrophil membrane serves as the first event in a complex signal transduction sequence involving activation of phospholipase C, which generates two second messengers, inositol 1,4,5-triphosphate (IP3) and diacylglycerol.…”

Section: Discussionmentioning

confidence: 99%

Persistance et voie de l’inhibition de la production de superoxyde par les neutrophiles induite par isoflurane

Saad

Eom

et al. 2009

Can J Anesth/J Can Anesth

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Background Our previous work has demonstrated that treatment with isoflurane has a preconditioning-like inhibitory effect on superoxide production (SOP) by polymorphonuclear neutrophils. The current objectives were to determine persistency of this effect and to clarify where in the signalling pathway this inhibition of SOP occurred. The latter was accomplished using two receptor-dependent neutrophil agonists, platelet activating factor (PAF) and formyl-methionyl-leucyl-phenylalanine (fMLP), and two receptor-independent neutrophil stimuli, the protein-kinase C stimulator, phorbol myristate acetate (PMA), and the calcium ionophore, A23187.Methods Arterial blood samples were obtained from eight dogs under baseline condition (conscious state), during isoflurane (1 MAC) administration, and 24 and 48 hr post-isoflurane (also in conscious state). Neutrophils were isolated and stimulated with 1 lM concentrations of PAF, fMLP, PMA, and A23187. SOP was measured spectrophotometrically. Results Isoflurane administration caused (1) an approximate 50% decrease in SOP during PAF or fMLP (P \ 0.01 vs baseline), which remained evident from 24 to 48 hr following isoflurane; (2) an initial 29% decrease in SOP during PMA (P \ 0.05 vs baseline), which returned to baseline by 24 hr following isoflurane; and (3) no change in SOP during A23187 (P [ 0.05 vs baseline). Conclusions Isoflurane administration caused prolonged (from 24 to 48 hr) decreases in agonist-induced SOP by neutrophils. This effect involved inhibition at site(s)

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Common and distinct intracellular signaling pathways in human neutrophils utilized by platelet activating factor and FMLP.

Cited by 292 publications

References 56 publications

Examination of the signal transduction pathways leading to activation of extracellular signal‐regulated kinase by formyl‐methionyl‐leucyl‐phenylalanine in rat neutrophils

Examination of the signal transduction pathways leading to activation of extracellular signal‐regulated kinase by formyl‐methionyl‐leucyl‐phenylalanine in rat neutrophils

Interaction between neurone and microglia mediated by platelet‐activating factor

Persistance et voie de l’inhibition de la production de superoxyde par les neutrophiles induite par isoflurane

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