Synergistic action of protein kinase C and calcium for histamine release from rat peritoneal mast cells

Katakami, Yuko; Kaibuchi, Kozo; Sawamura, Makoto; Takai, Yoshimi; Nishizuka, Yasutomi

doi:10.1016/0006-291x(84)90220-1

Cited by 171 publications

(44 citation statements)

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“…: 301-496-5639; Fax: 301-402-1542; E-mail: db225a@nih.gov. 1 The abbreviations used are: PKC, protein kinase C; NMHC, nonmuscle myosin heavy chain; CaM kinase, calcium/calmodulin-dependent protein kinase; PMA, phorbol 12-myristate 13-acetate; GF109203X, 2-[1-(3-dimethylaminopropyl)1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimide; BAPTA-AM, 1,2-bis(O-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid tetra(acetoxymethyl)ester; KN-92, 2-[N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzyl-amine phosphate; …”

Section: Methodsmentioning

confidence: 99%

“…Stimulation of sensitized mast cells by antigen leads to the activation of signal transduction pathways including signals generated through the mobilization of calcium and PKC 1 (1)(2)(3). One of the responses to these signals is the fusion of secretory granules with the plasma membrane, allowing release of preformed mediators such as histamine and serotonin from the cell.…”

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confidence: 99%

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Calcium-dependent Threonine Phosphorylation of Nonmuscle Myosin in Stimulated RBL-2H3 Mast Cells

Buxton

Adelstein

2000

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Calcium-dependent Threonine Phosphorylation of Nonmuscle Myosin in Stimulated RBL-2H3 Mast Cells

Buxton

Adelstein

2000

Journal of Biological Chemistry

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“…The early activation of PLCc1 results in the generation of inositol 1,4,5-triphosphate (IP 3 ) and diacylglycerol. These two second messengers lead to increases in cytoplasmic calcium and activation of calcium/diacylglycerol-regulated isoforms of protein kinase C (PKC) which culminate in granule margination and exocytosis [7]. PI3K plays an important regulatory role as an upstream activator of PLCc1, as well as a regulator of calcium flux during mast cell degranulation [8][9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Phospholipase Cγ negatively regulates Rac/Cdc42 activation in antigen‐stimulated mast cells

El‐Sibai

Backer

2006

Eur J Immunol

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The Rho GTPases Rac and Cdc42 play a central role in the regulation of secretory and cytoskeletal responses in antigen-stimulated mast cells. In this study, we examine the kinetics and mechanism of Rac and Cdc42 activation in the rat basophilic leukemia RBL-2H3 cells. The activation kinetics of both Rac and Cdc42 show a biphasic profile, consisting of an early transient peak at 1 min and a late sustained activation phase at 20-40 min. The inhibition of phospholipase C (PLC)c causes a twofold increase in Rac and Cdc42 activation that coincides with a dramatic production of atypical filopodialike structures. Inhibition of protein kinase C using bisindolylmaleimide mimics the effect of PLCc inhibition on Rac activation, but not on Cdc42 activation. In contrast, depletion of intracellular calcium leads to a complete inhibition of the early activation peak of both Rac and Cdc42, without significant effects on the late sustained activation. These data suggest that PLCc is involved in a negative feedback loop that leads to the inhibition of Rac and Cdc42. They also suggest that the presence of intracellular calcium is a prerequisite for both Rac and Cdc42 activation. IntroductionMast cells participate in the pathogenesis of immediate hypersensitivity and allergic reactions in humans [1]. Moreover, mast cells are important contributors to airway hyper-responsiveness that occurs in asthmatic inflammation [2]. In response to allergens and other exogenous stimuli, mast cells accumulate in the airway smooth muscle and in the bronchial intraepithelial layer [3]. The activation of mast cells, through the crosslinking of the FceRI, leads to the release of pre-formed early-phase inflammatory mediators and vasoactive substances from granules. It also leads to the in situ production of cytokines and bioactive lipids that contribute to the late-phase manifestation of the asthmatic reaction [4].Aggregation of FceRI on the surface of mast cells in response to multivalent ligand binding initiates a cascade of downstream signaling effectors that leads to degranulation [5]. These include phosphatidylinositol 3-kinase (PI3K), the guanine nucleotide exchange factor Vav, and phospholipase C (PLC)c1 [6]. The early activation of PLCc1 results in the generation of inositol 1,4,5-triphosphate (IP 3 ) and diacylglycerol. These two second messengers lead to increases in cytoplasmic calcium and activation of calcium/diacylglycerol-regulated isoforms of protein kinase C (PKC) which culminate in granule margination and exocytosis [7]. PI3K plays an important regulatory role as an upstream activator of PLCc1, as well as a regulator of calcium flux during mast cell degranulation [8][9][10][11][12][13].Members of the Rho family of small GTPases also regulate signaling events in mast cells [14][15][16]. In the rat basophilic leukemia (RBL-2H3) cells, Rac and Cdc42 have been implicated in the control of the FceRImediated phagocytosis and the regulation of migration, In conjunction with the secretory response, antigenstimulated mast cells undergo drama...

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“…When TPA was used to activate kinase C, first evidence indicated that calcium as an intracellular second messenger interacted synergistically with activated kinase C to initiate histamine secretion (Katakami et al, 1984). Partially purified kinase C has been isolated from the histamine-containing rat basophilic leukaemia cells .…”

Section: Discussionmentioning

confidence: 99%

“…histamine secretion induced by anti-IgE or A23187 plus TPA is greater than the sum of the histamine secreted in response to TPA and either anti-IgE or A23187 added separately (Katakami et al, 1984;Heiman & Crews, 1985;Cantwell & Foreman, 1986). Also, TPA produces histamine secretion in the absence of a receptor-ligand interaction at the cell membrane but in this case the secretion is slow, taking 90 min to reach maximum (Cantwell & Foreman, 1987).…”

Section: Introductionmentioning

confidence: 99%

The actions of inhibitors of diacylglycerol kinase and diacylglycerol lipase on histamine release from rat peritoneal mast cells

Cantwell

Foreman

1987

British J Pharmacology

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1 RHC 80267 and R59 022 are selective inhibitors of diacylglycerol (DAG) lipase and DAG kinase enzymes respectively. These inhibitors were examined with regard to their effects on oleoylacetylglycerol (OAG)-and anti-IgE-induced histamine secretion in rat peritoneal mast cells. 2 RHC 80267, 10 jiM and R59 022, 50 gM both enhanced OAG-induced histamine release by 30% and 40% respectively. 3 In the concentration range 3 -30 jM, R59 022 enhanced anti-IgE-induced histamine release by up to about 40%, whereas RHC 80267 was without effect. 4 The enhancement of anti-IgE-induced histamine release by R59 022 is consistent with a role for protein kinase C in transducing immunological signals to rat peritoneal mast cells. 5 The lack of effect of RHC 80267 in this situation may indicate that in the mast cell, DAG kinase is more active than DAG lipase in degrading physiological levels of DAG.

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Synergistic action of protein kinase C and calcium for histamine release from rat peritoneal mast cells

Cited by 171 publications

References 20 publications

Calcium-dependent Threonine Phosphorylation of Nonmuscle Myosin in Stimulated RBL-2H3 Mast Cells

Calcium-dependent Threonine Phosphorylation of Nonmuscle Myosin in Stimulated RBL-2H3 Mast Cells

Phospholipase Cγ negatively regulates Rac/Cdc42 activation in antigen‐stimulated mast cells

The actions of inhibitors of diacylglycerol kinase and diacylglycerol lipase on histamine release from rat peritoneal mast cells

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