PKC phosphorylation disrupts gap junctional communication at G0/S phase in clone 9 cells

Mol Cell Biochem. 1997 Feb;167(1-2):41-9. doi: 10.1023/a:1006831114120.

Abstract

Gap junctional communication during the progression of cell cycle from quiescent G0 to S phase was examined in cultured clone 9 rat liver cells. The transfer of scrape-loaded fluorescent dye was suppressed immediately after the stimulation of cell cycle progression in a synchronized cell population. Northern blot analysis showed that the temporal disturbance of gap junctional communication in cells passing from G0 to S phase did not result from transcriptional down-regulation of connexin 43. It was also found that the PKC inhibitor, calphostin C, was able to restore intercellular communication in serum stimulated cells. Data suggest a control mechanism by PKC mediated phosphorylation in the regulation of gap junction function which is vulnerable to cell cycling. The loss of gap junctional communication correlated with the increased phosphorylation of connexin 43 on serine residues in clone 9 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Carbazoles*
  • Cell Communication / drug effects
  • Cell Communication / physiology
  • Cells, Cultured
  • Clone Cells
  • Connexin 43 / genetics
  • Connexin 43 / immunology
  • Connexin 43 / metabolism
  • Enzyme Inhibitors / pharmacology
  • Fluorescent Dyes
  • Gap Junctions / drug effects
  • Gap Junctions / metabolism*
  • Imidazoles / pharmacology
  • Indoles / pharmacology
  • Liver / cytology*
  • Liver / drug effects
  • Liver / metabolism
  • Naphthalenes / pharmacology
  • Phosphorus Radioisotopes
  • Phosphorylation
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism*
  • Pyrroles / pharmacology
  • Rats
  • Resting Phase, Cell Cycle / drug effects
  • Resting Phase, Cell Cycle / physiology*
  • S Phase / drug effects
  • S Phase / physiology*
  • Transcription, Genetic

Substances

  • Carbazoles
  • Connexin 43
  • Enzyme Inhibitors
  • Fluorescent Dyes
  • Imidazoles
  • Indoles
  • Naphthalenes
  • Phosphorus Radioisotopes
  • Pyrroles
  • calmidazolium
  • KT 5720
  • Protein Kinase C
  • Calcium-Calmodulin-Dependent Protein Kinases
  • calphostin C