Respiratory burst in activated neutrophils is directly correlated to the intracellular level of protein kinase C

Salamino, Franca; Sparatore, Bianca; Tullio, Roberta De; Mengotti, P.; Melloni, Edon; Pontremoli, S.

doi:10.1111/j.1432-1033.1991.tb16220.x

Cited by 15 publications

(3 citation statements)

References 27 publications

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“…We therefore suggest that fMLP-triggered PMN functions are linked to PKC isotypes but are able to coopt alternative fMLP-sensitive signal pathways for ROS formation. This does not apply to PMA-triggered oxidative activity as this has been shown to be susceptible to H7 [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Polymorphonuclear Cell Chemotaxis and Suicidal NETosis: Simultaneous Observation Using fMLP, PMA, H7, and Live Cell Imaging

Pai

Gruber

Pfaehler

et al. 2020

Journal of Immunology Research

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Chemotaxis and the formation of suicidal neutrophil extracellular traps (suicidal NETosis) are key functions of polymorphonuclear cells (PMNs). Neutrophil extracellular traps in particular are known to be significantly involved in the severity of inflammatory and immunological disorders such as rheumatoid arthritis and Crohn’s disease. Therefore, detailed knowledge of PMNs is essential for analyzing the mechanisms involved in, and developing new therapies for, such diseases. To date, no standard method to analyze these cell activities has been established. This study used in vitro live cell imaging to simultaneously observe and analyze PMN functions. To demonstrate this, the effects of phorbol-12-myristat-13-acetat (PMA, 0.1-10 nM), N-formylmethionine-leucyl-phenylalanine (fMLP, 10 nM), and protein kinase C inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7) on PMN chemotaxis and suicidal NETosis were studied. PMA (1 nM-10 nM) resulted in significant concentration-dependent behavior in chemotaxis and an earlier onset of maximum oxidative burst and NET formation of up to 44%. When adding H7, PMA-triggered PMN functions were reduced, demonstrating that all three functions rely mostly on protein kinase C (PKC) activity, while PKC is not essential for fMLP-induced PMN activity. Thus, the method here described can be used to objectively quantify PMN functions and, especially through the regulation of the PKC pathway, could be useful in further clinical studies of immunological disorders.

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Section: Discussionmentioning

confidence: 99%

Polymorphonuclear Cell Chemotaxis and Suicidal NETosis: Simultaneous Observation Using fMLP, PMA, H7, and Live Cell Imaging

Pai

Gruber

Pfaehler

et al. 2020

Journal of Immunology Research

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“…In neutrophils 18 and Ehrlich ascites tumor cells, 30 O 2~ production has been repeatedly stimulated by administration of tumorpromoting phorbol compounds known to activate protein kinase C. This has also been demonstrated in cultured endothelial cells. 19 The production of O 2~ by neutrophils is proportional to the activity of intracellular protein kinase C. 31 Lyso-PC, in the presence of diacylglycerol and phosphatidylserine, can activate protein kinase C at physiological calcium concentrations. 32 Conversely, lyso-PC, in the presence of calcium and phosphatidylserine, can potentiate the effect of diacylglycerol in activating protein kinase C. 13 Protein phosphorylation and activation of an NADPH oxidase are probably involved in the ultimate pathway leading to O 2~ production.…”

Section: Discussionmentioning

confidence: 99%

Lysophosphatidylcholine increases vascular superoxide anion production via protein kinase C activation.

Ohara

Peterson

Zheng

et al. 1994

Arterioscler Thromb

126

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We tested the hypothesis that lysophosphatidylcholine (lyso-PC) could activate protein kinase C in intact vascular segments and sought to examine some of the physiological consequences of this activation. In segments of rabbit aorta, the patterns of protein phosphorylation determined by two-dimensional electrophoresis stimulated by lyso-PC and 12-0-tetradecanoylphorbol 13-acetate (TPA) were similar. Activation of protein kinase C can stimulate superoxide anion (O 2~) production in other tissues, and we found that lyso-PCtreated rabbit aortas produced twofold more O 2~ than control vessels. Calphostin C, a potent and specific inhibitor of protein kinase C, attenuated O 2~ production in lyso-PC-treated vessels but had no effect in control vessels. The effect of lyso-PC on O 2~ production was mimicked by TPA. In separate bioassay studies, release of the endothelium-derived vascular relaxing S everal lines of evidence have indicated that oxidatively modified low-density lipoprotein (LDL) plays a central role in atherogenesis.

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“…PKC activity is one of the rate-limiting factors of the respiratory burst activity. It has been reported that the neutrophil respiratory burst correlates directly with the intracellular level of PKC (56). Moreover, PKC inhibitors such as staurosporine and H-7 inhibit both phosphorylation of 47-kDa protein and superoxide production in a dose-dependent manner (57).…”

Section: Discussionmentioning

confidence: 99%

Monochloramine Inhibits Phorbol Ester-inducible Neutrophil Respiratory Burst Activation and T Cell Interleukin-2 Receptor Expression by Inhibiting Inducible Protein Kinase C Activity

Ogino

Kobuchi

Sen

et al. 1997

Journal of Biological Chemistry

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Monochloramine derivatives are long lived physiological oxidants produced by neutrophils during the respiratory burst. The effects of chemically prepared monochloramine (NH 2 Cl) on protein kinase C (PKC) and PKCmediated cellular responses were studied in elicited rat peritoneal neutrophils and human Jurkat T cells. Neutrophils pretreated with NH 2 Cl (30 -50 M) showed a marked decrease in the respiratory burst activity induced by phorbol 12-myristate 13-acetate (PMA), which is a potent PKC activator. These cells, however, were viable and showed a complete respiratory burst upon arachidonic acid stimulation, which induces the respiratory burst by a PKC-independent mechanism. The NH 2 Cl-treated neutrophils showed a decrease in both PKC activity and PMA-induced phosphorylation of a 47-kDa protein, which corresponds to the cytosolic factor of NADPH oxidase, p47phox . Jurkat T cells pretreated with NH 2 Cl (20 -70 M) showed a decrease in the expression of the interleukin-2 receptor ␣ chain following PMA stimulation. This was also accompanied by a decrease in both PKC activity and nuclear transcription factor-B activation, also without loss of cell viability. These results show that NH 2 Cl inhibits PKC-mediated cellular responses through inhibition of the inducible PKC activity.

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Respiratory burst in activated neutrophils is directly correlated to the intracellular level of protein kinase C

Cited by 15 publications

References 27 publications

Polymorphonuclear Cell Chemotaxis and Suicidal NETosis: Simultaneous Observation Using fMLP, PMA, H7, and Live Cell Imaging

Polymorphonuclear Cell Chemotaxis and Suicidal NETosis: Simultaneous Observation Using fMLP, PMA, H7, and Live Cell Imaging

Lysophosphatidylcholine increases vascular superoxide anion production via protein kinase C activation.

Monochloramine Inhibits Phorbol Ester-inducible Neutrophil Respiratory Burst Activation and T Cell Interleukin-2 Receptor Expression by Inhibiting Inducible Protein Kinase C Activity

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