Expression and characterization of protein kinase C in isolated rabbit parietal cells.

Nandi, Jyotirmoy; Loo, A. A. J. van de; Kim, S W; Levine, R A

doi:10.3892/ijmm.3.5.521

Cited by 2 publications

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“…The importance of this regulation for parietal cell signaling and attenuation of H + secretion is currently unknown. Combining our data with recent reports (Nandi et al, 1999;Beales & Calam, 2001;Fa¨hrmann et al, 2002a,b), it becomes more obvious that PKC-a plays a suppressive rather than obligatory role in the signal transduction of parietal cells. Figure 6 Autophosphorylation sites of CaMKII.…”

Section: Discussionsupporting

confidence: 88%

“…Most of these reports indicate an attenuating rather than facilitating function of PKC in acetylcholine-mediated acid secretion at the level of parietal cells. Especially for the calcium-dependent PKC-a, an inhibitory role in parietal cells has been suggested (Nandi et al, 1999;Fa¨hrmann et al, 2002b). In contrast to this, CaMKII appears to play the role of an important mediator in cholinergic signal transduction for acid secretion.…”

Section: Discussionmentioning

confidence: 99%

“…The generated inositol trisphosphate mobilizes Ca 2+ from the endoplasmatic reticulum. In parietal cells, free intracellular Ca 2+ stimulates signalling pathways involving protein kinase C (PKC) (Brown & Chew, 1987;Chiba et al, 1989;Nandi et al, 1996;reviewed in Fa¨hrmann, 2000) and Ca 2+ / calmodulin-dependent protein kinase II (CaMKII) (Tsunoda et al, 1992;Fa¨hrmann et al, 2002a,b), respectively, which are both abundant in gastric parietal cells (Mayer et al, 1994;Nandi et al, 1996Nandi et al, , 1999Chew et al, 1997;Fa¨hrmann et al, 1998;2002a;Fa¨hrmann & Pfeiffer, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Protein kinase C‐α attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells

Fährmann

Kaufhold

Pfeiffer³

et al. 2003

British J Pharmacology

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1 The phorbolester 12-O-tetradecanoyl phorbol-13-acetate (TPA), an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion. We observed that this effect strongly correlated with the inhibition of Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) activity in rabbit parietal cells. 2 The aim of this study was to specify the function of PKC-a in cholinergically stimulated H + secretion. PKC-a represents the only calcium-dependent PKC isoenzyme that has been detected in rabbit parietal cells. 3 Go¨6976, an inhibitor of calcium-dependent PKC, concentration-dependently antagonized the inhibitory effect of TPA, and, therefore, revealed the action of PKC-a on carbachol-induced acid secretion in rabbit parietal cells. 4 TPA exerted no additive inhibition of carbachol-stimulated acid secretion if acid secretion was partially inhibited by the potent CaMKII inhibitor 1-[N,O-bis(5-isoquinolinsulfonyl)-N-methyl-L-tyrosyl]-4-phenyl-piperazine (KN-62). 5 Since both kinase modulators, TPA and KN-62, affected no divergent signal transduction pathways in the parietal cell, an in vitro model has been used to study if PKC directly targets CaMKII. CaMKII purified from parietal cell-containing gastric mucosa of pig, was transphosphorylated by purified cPKC containing PKC-a up to 1.8 mol P i per mol CaMKII in vitro. The autonomy site of CaMKII was not transphosphorylated by PKC. 6 The phosphotransferase activity of the purified CaMKII was in vitro inhibited after transphosphorylation by PKC if calmodulin was absent during transphosphorylation. Attenuation of CaMKII activity by PKC showed strong similarity to the downregulation of CaMKII by basal autophosphorylation. 7 Our results suggest that PKC-a and CaMKII are closely functionally linked in a cholinergically induced signalling pathway in rabbit parietal cells. We assume that in cholinergically stimulated parietal cells PKC-a transinhibits CaMKII activity, resulting in an attenuation of acid secretion.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protein kinase C‐α attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells

Fährmann

Kaufhold

Pfeiffer³

et al. 2003

British J Pharmacology

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“…Furthermore, the potentiating actions of salicylate and non‐salicylate non‐specific NSAIDs are calcium dependent and associated with increased calcium efflux in parietal cells 8,9 . It is possible that NSAID‐induced augmentation of gastric acid secretion mediated via protein kinase C 20–22 may lead to enhanced proton pump expression. This possibility should be investigated further.…”

Section: Discussionmentioning

confidence: 99%

“…However, it remains unknown whether COX‐1 and/or COX‐2 inhibition can modulate gastric acid secretion. Previous data 8,9 indicate that NSAID potentiation of secretagogue‐stimulated acid secretion in rabbit parietal cells is located at a post‐receptor site prior to the H + /K + ‐ATPase, dependent on extracellular calcium, independent of pertussis‐sensitive GTP‐binding proteins and histamine and muscarinic receptor activation, and possibly regulated by protein kinase C 20–22 …”

Section: Introductionmentioning

confidence: 99%

CYCLO‐OXYGENASE‐1 INHIBITION INCREASES ACID SECRETION BY MODULATING H⁺,K⁺‐ATPase EXPRESSION AND ACTIVATION IN RABBIT PARIETAL CELLS

Nandi¹,

Das²,

Zinkievich³

et al. 2009

Clin Exp Pharma Physio

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1. In the present study, we evaluated the role of cyclo-oxygenase (COX)-1 and COX-2 on gastric acid secretion in rabbit isolated parietal cells and gastric glands by examining [(14)C]-aminopyrine uptake, prostaglandin (PG) E(2) synthesis and COX-1, COX-2 and proton pump expression at baseline and after treatment with various concentrations of specific COX-1 (SC-560), COX-2 (5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methyl-sulphonyl)phenyl-2 (5H)-furanone; DFU) and non-specific COX (indomethacin) inhibitors. 2. In parietal cells, SC-560 and indomethacin, over the concentration range 10(-8) to 10(-4) mol/L, dose-dependently increased basal and 10(-4) mol/L histamine-stimulated aminopyrine uptake and inhibited PGE(2) synthesis, whereas DFU (10(-8) to 10(-5) mol/L) had no effect. However, at 10(-4) mol/L, DFU augmented histamine-stimulated aminopyrine uptake by 135% and inhibited PGE(2) synthesis by 39%, indicating an inhibition of COX-1 at this higher concentration. 3. The SC-560-, DFU- and indomethacin-induced augmentation of histamine-stimulated aminopyrine uptake was reduced to basal levels after 10(-5) mol/L lansoprazole treatment in parietal cells and gastric glands, whereas 10(-4) mol/L ranitidine only partially inhibited such augmentation. 4. Only COX-1 was detected in parietal cells. However, both COX-1 and COX-2 were expressed in gastric glands, with relative protein density of COX-1 being sixfold higher than that of COX-2. Protein levels of COX-1 in parietal cells and those of COX-1 and COX-2 in gastric glands remained unchanged, regardless of inhibitor treatment, either alone or with histamine. 5. Parietal cell proton pump expression was significantly enhanced by 10(-5) mol/L SC-560 and 10(-4) mol/L indomethacin (by 29 and 31%, respectively) and pump activity was enhanced by 61 and 65%, respectively. In contrast, 10(-5) mol/L DFU had no effect. 6. In conclusion, the data indicate that inhibition of COX-1- but not COX-2-derived PGE(2) synthesis is involved in augmentation of non-steroidal anti-inflammatory drug-induced gastric acid secretion in parietal cells by enhancing expression and activation of the proton pump.

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Expression and characterization of protein kinase C in isolated rabbit parietal cells.

Cited by 2 publications

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Protein kinase C‐α attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells

Protein kinase C‐α attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells

CYCLO‐OXYGENASE‐1 INHIBITION INCREASES ACID SECRETION BY MODULATING H⁺,K⁺‐ATPase EXPRESSION AND ACTIVATION IN RABBIT PARIETAL CELLS

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Expression and characterization of protein kinase C in isolated rabbit parietal cells.

Cited by 2 publications

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Protein kinase C‐α attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells

Protein kinase C‐α attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells

CYCLO‐OXYGENASE‐1 INHIBITION INCREASES ACID SECRETION BY MODULATING H+,K+‐ATPase EXPRESSION AND ACTIVATION IN RABBIT PARIETAL CELLS

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CYCLO‐OXYGENASE‐1 INHIBITION INCREASES ACID SECRETION BY MODULATING H⁺,K⁺‐ATPase EXPRESSION AND ACTIVATION IN RABBIT PARIETAL CELLS