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Different actions of protein kinase C isoforms α and ε on gastric acid secretion
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| Zeitschriftentitel: | British Journal of Pharmacology |
|---|---|
| Personen und Körperschaften: | , , , |
| In: | British Journal of Pharmacology, 136, 2002, 6, S. 938-946 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Fährmann, Michael Kaufhold, Marc Rieg, Timo Seidler, Ursula Fährmann, Michael Kaufhold, Marc Rieg, Timo Seidler, Ursula |
|---|---|
| author |
Fährmann, Michael Kaufhold, Marc Rieg, Timo Seidler, Ursula |
| spellingShingle |
Fährmann, Michael Kaufhold, Marc Rieg, Timo Seidler, Ursula British Journal of Pharmacology Different actions of protein kinase C isoforms α and ε on gastric acid secretion Pharmacology |
| author_sort |
fährmann, michael |
| spelling |
Fährmann, Michael Kaufhold, Marc Rieg, Timo Seidler, Ursula 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1038/sj.bjp.0704790 <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>The phorbol ester TPA, an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion but increases basal H<jats:sup>+</jats:sup> secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Since these contradictory findings suggest the action of different PKC isozymes we analysed the role of calcium‐dependent PKC‐α, and calcium‐independent PKC‐ε in gastric acid secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Inhibition of PKC‐α by the indolocarbazole Gö 6976 revealed that about 28% of carbachol‐induced acid secretion was inhibited by PKC‐α. In the presence of Gö 6976 approximately 64% of the carbachol‐induced signal transduction is mediated by Ca<jats:sup>2+</jats:sup>/calmodulin‐dependent protein kinase II (CaMKII), and 14% is conveyed by PKC‐ε as deduced from the inhibition with the bisindolylmaleimide Ro 31‐8220.</jats:p></jats:list-item> <jats:list-item><jats:p>Inhibition of carbachol‐induced acid secretion by TPA was accompanied by a decrease in CaMKII activity.</jats:p></jats:list-item> <jats:list-item><jats:p>The stimulation of basal acid secretion by TPA was biphasic with a peak at a very low concentration (10 p<jats:sc>M</jats:sc>), resulting in an activation of the calcium‐sensor CaMKII. The activation was determined with a phosphospecific polyclonal antibody against active CaMKII. The TPA‐induced increase of H<jats:sup>+</jats:sup> secretion was sensitive to the cell‐permeable Ca<jats:sup>2+</jats:sup>‐chelator BAPTA/AM, Ro 31‐8220, and the CaMKII‐inhibitor KN‐62, but not to Gö 6976.</jats:p></jats:list-item> <jats:list-item><jats:p>Since TPA induced the translocation of PKC‐ε but not of PKC‐α in resting parietal cells, PKC‐ε seems to be at least responsible for an initial elevation of free intracellular calcium to initiate TPA‐induced acid secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Our data indicate the different roles of two PKC isoforms: PKC‐ε activation appears to facilitate cholinergic stimulation of H<jats:sup>+</jats:sup>‐secretion likely by increasing intracellular calcium. In contrast, PKC‐α activation attenuates acid secretion accompanied by a down‐regulation of CaMKII activity.</jats:p></jats:list-item> </jats:list> </jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (2002) <jats:bold>136</jats:bold>, 938–946. doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0704790">10.1038/sj.bjp.0704790</jats:ext-link></jats:p> Different actions of protein kinase C isoforms α and ε on gastric acid secretion British Journal of Pharmacology |
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Chemie und Pharmazie |
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Wiley, 2002 |
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2002 |
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Wiley |
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British Journal of Pharmacology |
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49 |
| title |
Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_unstemmed |
Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_full |
Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_fullStr |
Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_full_unstemmed |
Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_short |
Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_sort |
different actions of protein kinase c isoforms α and ε on gastric acid secretion |
| topic |
Pharmacology |
| url |
http://dx.doi.org/10.1038/sj.bjp.0704790 |
| publishDate |
2002 |
| physical |
938-946 |
| description |
<jats:p>
<jats:list list-type="explicit-label">
<jats:list-item><jats:p>The phorbol ester TPA, an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion but increases basal H<jats:sup>+</jats:sup> secretion.</jats:p></jats:list-item>
<jats:list-item><jats:p>Since these contradictory findings suggest the action of different PKC isozymes we analysed the role of calcium‐dependent PKC‐α, and calcium‐independent PKC‐ε in gastric acid secretion.</jats:p></jats:list-item>
<jats:list-item><jats:p>Inhibition of PKC‐α by the indolocarbazole Gö 6976 revealed that about 28% of carbachol‐induced acid secretion was inhibited by PKC‐α. In the presence of Gö 6976 approximately 64% of the carbachol‐induced signal transduction is mediated by Ca<jats:sup>2+</jats:sup>/calmodulin‐dependent protein kinase II (CaMKII), and 14% is conveyed by PKC‐ε as deduced from the inhibition with the bisindolylmaleimide Ro 31‐8220.</jats:p></jats:list-item>
<jats:list-item><jats:p>Inhibition of carbachol‐induced acid secretion by TPA was accompanied by a decrease in CaMKII activity.</jats:p></jats:list-item>
<jats:list-item><jats:p>The stimulation of basal acid secretion by TPA was biphasic with a peak at a very low concentration (10 p<jats:sc>M</jats:sc>), resulting in an activation of the calcium‐sensor CaMKII. The activation was determined with a phosphospecific polyclonal antibody against active CaMKII. The TPA‐induced increase of H<jats:sup>+</jats:sup> secretion was sensitive to the cell‐permeable Ca<jats:sup>2+</jats:sup>‐chelator BAPTA/AM, Ro 31‐8220, and the CaMKII‐inhibitor KN‐62, but not to Gö 6976.</jats:p></jats:list-item>
<jats:list-item><jats:p>Since TPA induced the translocation of PKC‐ε but not of PKC‐α in resting parietal cells, PKC‐ε seems to be at least responsible for an initial elevation of free intracellular calcium to initiate TPA‐induced acid secretion.</jats:p></jats:list-item>
<jats:list-item><jats:p>Our data indicate the different roles of two PKC isoforms: PKC‐ε activation appears to facilitate cholinergic stimulation of H<jats:sup>+</jats:sup>‐secretion likely by increasing intracellular calcium. In contrast, PKC‐α activation attenuates acid secretion accompanied by a down‐regulation of CaMKII activity.</jats:p></jats:list-item>
</jats:list>
</jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (2002) <jats:bold>136</jats:bold>, 938–946. doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0704790">10.1038/sj.bjp.0704790</jats:ext-link></jats:p> |
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| description | <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>The phorbol ester TPA, an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion but increases basal H<jats:sup>+</jats:sup> secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Since these contradictory findings suggest the action of different PKC isozymes we analysed the role of calcium‐dependent PKC‐α, and calcium‐independent PKC‐ε in gastric acid secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Inhibition of PKC‐α by the indolocarbazole Gö 6976 revealed that about 28% of carbachol‐induced acid secretion was inhibited by PKC‐α. In the presence of Gö 6976 approximately 64% of the carbachol‐induced signal transduction is mediated by Ca<jats:sup>2+</jats:sup>/calmodulin‐dependent protein kinase II (CaMKII), and 14% is conveyed by PKC‐ε as deduced from the inhibition with the bisindolylmaleimide Ro 31‐8220.</jats:p></jats:list-item> <jats:list-item><jats:p>Inhibition of carbachol‐induced acid secretion by TPA was accompanied by a decrease in CaMKII activity.</jats:p></jats:list-item> <jats:list-item><jats:p>The stimulation of basal acid secretion by TPA was biphasic with a peak at a very low concentration (10 p<jats:sc>M</jats:sc>), resulting in an activation of the calcium‐sensor CaMKII. The activation was determined with a phosphospecific polyclonal antibody against active CaMKII. The TPA‐induced increase of H<jats:sup>+</jats:sup> secretion was sensitive to the cell‐permeable Ca<jats:sup>2+</jats:sup>‐chelator BAPTA/AM, Ro 31‐8220, and the CaMKII‐inhibitor KN‐62, but not to Gö 6976.</jats:p></jats:list-item> <jats:list-item><jats:p>Since TPA induced the translocation of PKC‐ε but not of PKC‐α in resting parietal cells, PKC‐ε seems to be at least responsible for an initial elevation of free intracellular calcium to initiate TPA‐induced acid secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Our data indicate the different roles of two PKC isoforms: PKC‐ε activation appears to facilitate cholinergic stimulation of H<jats:sup>+</jats:sup>‐secretion likely by increasing intracellular calcium. In contrast, PKC‐α activation attenuates acid secretion accompanied by a down‐regulation of CaMKII activity.</jats:p></jats:list-item> </jats:list> </jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (2002) <jats:bold>136</jats:bold>, 938–946. doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0704790">10.1038/sj.bjp.0704790</jats:ext-link></jats:p> |
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| spelling | Fährmann, Michael Kaufhold, Marc Rieg, Timo Seidler, Ursula 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1038/sj.bjp.0704790 <jats:p> <jats:list list-type="explicit-label"> <jats:list-item><jats:p>The phorbol ester TPA, an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion but increases basal H<jats:sup>+</jats:sup> secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Since these contradictory findings suggest the action of different PKC isozymes we analysed the role of calcium‐dependent PKC‐α, and calcium‐independent PKC‐ε in gastric acid secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Inhibition of PKC‐α by the indolocarbazole Gö 6976 revealed that about 28% of carbachol‐induced acid secretion was inhibited by PKC‐α. In the presence of Gö 6976 approximately 64% of the carbachol‐induced signal transduction is mediated by Ca<jats:sup>2+</jats:sup>/calmodulin‐dependent protein kinase II (CaMKII), and 14% is conveyed by PKC‐ε as deduced from the inhibition with the bisindolylmaleimide Ro 31‐8220.</jats:p></jats:list-item> <jats:list-item><jats:p>Inhibition of carbachol‐induced acid secretion by TPA was accompanied by a decrease in CaMKII activity.</jats:p></jats:list-item> <jats:list-item><jats:p>The stimulation of basal acid secretion by TPA was biphasic with a peak at a very low concentration (10 p<jats:sc>M</jats:sc>), resulting in an activation of the calcium‐sensor CaMKII. The activation was determined with a phosphospecific polyclonal antibody against active CaMKII. The TPA‐induced increase of H<jats:sup>+</jats:sup> secretion was sensitive to the cell‐permeable Ca<jats:sup>2+</jats:sup>‐chelator BAPTA/AM, Ro 31‐8220, and the CaMKII‐inhibitor KN‐62, but not to Gö 6976.</jats:p></jats:list-item> <jats:list-item><jats:p>Since TPA induced the translocation of PKC‐ε but not of PKC‐α in resting parietal cells, PKC‐ε seems to be at least responsible for an initial elevation of free intracellular calcium to initiate TPA‐induced acid secretion.</jats:p></jats:list-item> <jats:list-item><jats:p>Our data indicate the different roles of two PKC isoforms: PKC‐ε activation appears to facilitate cholinergic stimulation of H<jats:sup>+</jats:sup>‐secretion likely by increasing intracellular calcium. In contrast, PKC‐α activation attenuates acid secretion accompanied by a down‐regulation of CaMKII activity.</jats:p></jats:list-item> </jats:list> </jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (2002) <jats:bold>136</jats:bold>, 938–946. doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0704790">10.1038/sj.bjp.0704790</jats:ext-link></jats:p> Different actions of protein kinase C isoforms α and ε on gastric acid secretion British Journal of Pharmacology |
| spellingShingle | Fährmann, Michael, Kaufhold, Marc, Rieg, Timo, Seidler, Ursula, British Journal of Pharmacology, Different actions of protein kinase C isoforms α and ε on gastric acid secretion, Pharmacology |
| title | Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_full | Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_fullStr | Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_full_unstemmed | Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_short | Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| title_sort | different actions of protein kinase c isoforms α and ε on gastric acid secretion |
| title_unstemmed | Different actions of protein kinase C isoforms α and ε on gastric acid secretion |
| topic | Pharmacology |
| url | http://dx.doi.org/10.1038/sj.bjp.0704790 |