1,25(OH)2-vitamin D3 affects the subcellular distribution of protein kinase C isoenzymes in rat duodenum: Influence of aging

Balogh, Gabriela Andrea; Boland, Ricardo; Boland, Ana Russo de

doi:10.1002/1097-4644(20001215)79:4<686::aid-jcb160>3.0.co;2-p

Cited by 15 publications

(12 citation statements)

References 32 publications

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“…These multiple roles suggest that this group of enzymes is involved in the regulation of the health and damage of epithelial cells and the intestinal barrier. Thus, it is not surprising that these enzymes are modified by a wide variety of physical and physiological stimuli such as age (Balogh et al, 2000), diet (Murray et al, 2002), and hormones (Balogh et al, 2000). Nevertheless, the de-tailed mechanisms by which PKC isoforms are involved in these vital pathways remains to be elucidated.…”

Section: Protein Kinasesmentioning

confidence: 99%

The Role of Protein Kinase C Isoforms in Modulating Injury and Repair of the Intestinal Barrier

Farhadi¹,

Keshavarzian²,

Ranjbaran³

et al. 2005

J Pharmacol Exp Ther

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Section: Protein Kinasesmentioning

confidence: 99%

The Role of Protein Kinase C Isoforms in Modulating Injury and Repair of the Intestinal Barrier

Farhadi¹,

Keshavarzian²,

Ranjbaran³

et al. 2005

J Pharmacol Exp Ther

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“…PKC␤ and -␦ were not detected in duodenal mucosa in mice. The study of Balogh et al (1), however, showed that PKC␣, -␤, and -␦, but not PKC⑀ and -were expressed in rat duodenal mucosa. This discrepancy may be related to species or to methodological differences.…”

Section: Discussionmentioning

confidence: 99%

Protein kinase C potentiates cAMP-stimulated mouse duodenal mucosal bicarbonate secretion in vitro

Tuo

Chow

Barrett

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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; 10.1152/ajpgi.00251.2003.-PKC has been shown to regulate epithelial Cl Ϫ secretion in a variety of models. However, the role of PKC in duodenal mucosal bicarbonate secretion is less clear. We aimed to investigate the role of PKC in regulation of duodenal mucosal bicarbonate secretion. Bicarbonate secretion by murine duodenal mucosa was examined in vitro in Ussing chambers using a pH-stat technique. PKC isoform expression and activity were assessed by Western blotting and in vitro kinase assays, respectively. PMA (an activator of PKC) alone had no effect on duodenal bicarbonate secretion or short-circuit current (Isc). When PMA and dibutyrylcAMP (db-cAMP) were added simultaneously, PMA failed to alter db-cAMP-stimulated duodenal bicarbonate secretion or Isc (P Ͼ 0.05). However, a 1-h preincubation with PMA potentiated db-cAMPstimulated duodenal bicarbonate secretion and Isc in a concentrationdependent manner (from 10 Ϫ8 to 10 Ϫ5 M) (P Ͻ 0.05). PMA preincubation had no effects on carbachol-or heat-stable toxin-stimulated bicarbonate secretion. Western blot analysis revealed that PKC␣, -␥, -⑀, -, -, and -/ were expressed in murine duodenal mucosa. Ro 31-8220 (an inhibitor active against PKC⑀, -␣, -␤, and -␥), but not Gö 6983 (an inhibitor active against PKC␣, -␥, -␤, and -␦), reversed the potentiating effect of PMA on db-cAMP-stimulated bicarbonate secretion. PMA also time-and concentration-dependently increased the activity of PKC⑀, an effect that was prevented by Ro 31-8220 but not Gö 6983. These results demonstrate that activation of PKC potentiates cAMP-stimulated duodenal bicarbonate secretion, whereas it does not modify basal secretion. The effect of PKC on cAMP-stimulated bicarbonate secretion is mediated by the PKC⑀ isoform.

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“…It is noteworthy that PKC-δ is also expressed in the duodenum (6,7) and that activation of duodenal mucosal PKC-δ inhibits glucose production (6). Although duodenal PKC-δ activation (6) or CCK action (2) is necessary for lipid sensing and sufficient to trigger a gut–brain–liver axis to lower glucose production, the interfunctional relationship between PKC-δ and CCK has yet to be established.…”

mentioning

confidence: 99%

Duodenal PKC-δ and Cholecystokinin Signaling Axis Regulates Glucose Production

et al. 2011

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OBJECTIVEMetabolism of long-chain fatty acids within the duodenum leads to the activation of duodenal mucosal protein kinase C (PKC)-δ and the cholecystokinin (CCK)-A receptor to lower glucose production through a neuronal network. However, the interfunctional relationship between duodenal PKC-δ and CCK remains elusive. Although long-chain fatty acids activate PKC to stimulate the release of CCK in CCK-secreting cells, CCK has also been found to activate PKC-δ in pancreatic acinar cells. We here evaluate whether activation of duodenal mucosal PKC-δ lies upstream (and/or downstream) of CCK signaling to lower glucose production.RESEARCH DESIGN AND METHODSWe first determined with immunofluorescence whether PKC-δ and CCK were colocalized within the duodenal mucosa. We then performed gain- and loss-of-function experiments targeting duodenal PKC-δ and the CCK-A receptor and evaluated the impact on changes in glucose kinetics during pancreatic (basal insulin) clamps in rats in vivo.RESULTSImmunostaining of PKC-δ was found to colocalize with CCK in the duodenal mucosa. Intraduodenal coinfusion of either the CCK-A receptor antagonist MK-329 or CR-1409 with the PKC activator negated the ability of duodenal mucosal PKC-δ activation to lower glucose production during the pancreatic clamps in normal rats. Conversely, molecular and pharmacological inhibition of duodenal PKC-δ did not negate the ability of the duodenal CCK-A receptor agonist CCK-8 to lower glucose production, indicating that activation of duodenal PKC-δ lies upstream (and not downstream) of CCK signaling. Finally, intraduodenal PKC activator infusion failed to lower glucose production in rats with high-fat diet–induced duodenal CCK resistance.CONCLUSIONSIn summary, activation of duodenal PKC-δ leads to the stimulation of CCK release and activation of the CCK-A receptor signaling axis to lower glucose production in normal rats, but fails to bypass duodenal CCK-resistance in high fat-fed rats.

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1,25(OH)2-vitamin D3 affects the subcellular distribution of protein kinase C isoenzymes in rat duodenum: Influence of aging

Cited by 15 publications

References 32 publications

The Role of Protein Kinase C Isoforms in Modulating Injury and Repair of the Intestinal Barrier

The Role of Protein Kinase C Isoforms in Modulating Injury and Repair of the Intestinal Barrier

Protein kinase C potentiates cAMP-stimulated mouse duodenal mucosal bicarbonate secretion in vitro

Duodenal PKC-δ and Cholecystokinin Signaling Axis Regulates Glucose Production

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