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Related Experiment Videos

Different pathways mediate cholecystokinin actions in cholelithiasis

Q Chen1, G De Petris, P Yu

  • 1Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence 02903, USA.

The American Journal of Physiology
|April 1, 1997
PubMed
Summary

Gallbladder muscle with cholesterol stones shows altered contraction signaling. Protein Kinase C (PKC) activation, not calmodulin, mediates cholecystokinin response in diseased gallbladders.

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Area of Science:

  • Gastroenterology
  • Cellular Physiology
  • Biochemistry

Background:

  • Gallbladder smooth muscle response to cholecystokinin (CCK) is impaired in the presence of cholesterol stones.
  • Understanding the underlying signal-transduction pathways is crucial for explaining this functional deficit.

Purpose of the Study:

  • To investigate the distinct signal-transduction pathways mediating CCK-induced gallbladder contraction in the presence of cholesterol stones.
  • To compare these pathways in prairie dog and human gallbladder models.

Main Methods:

  • Enzymatic isolation of gallbladder muscle cells for contraction studies.
  • Measurement of Protein Kinase C (PKC) activity via substrate peptide phosphorylation.
  • Assessment of CCK octapeptide (CCK-8) induced contraction and pathway antagonist effects.

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Main Results:

  • Gallbladder muscle from cholesterol-fed prairie dogs showed reduced CCK-8 contraction compared to controls.
  • While inositol-1,4,5-trisphosphate, diacylglycerol, and guanosine 5'-O-(3-thiotriphosphate) induced similar contractions in both groups.
  • Control gallbladders utilized a calmodulin-dependent pathway for CCK-8 contraction, whereas gallbladders with cholesterol stones relied on a PKC-dependent pathway, showing increased PKC translocation.

Conclusions:

  • CCK-8 activates calmodulin-dependent pathways in normal gallbladder muscle.
  • In gallbladders with cholesterol stones, CCK-8 activates PKC-dependent pathways.
  • The primary defect in gallbladder muscle associated with cholesterol stones may occur upstream of G protein activation.