Regulation of the MDCK cell tight junction

O. N. Kovbasnjuk, U. Szmulowicz, K. R. Spring

Research output: Contribution to journalArticlepeer-review

Abstract

The sodium flux across individual tight junctions (TJ) of low-resistance MDCK cell monolayers grown on glass coverslips was determined as a measure of paracellular permeability. increases in perfusate glucose concentration from 5 to 25 mM decreased tight junction Na permeability. This permeability decrease was not specific as nonmetabolizable analogues of glucose caused similar diminutions in TJ Na permeability. Stimulation of protein kinase A increased TJ Na permeability, and inhibition of protein kinase A decreased TJ Na permeability. Transepithelial electrical resistance of monolayers grown on permeable supports did not change as predicted from the observed alterations in TJ Na permeability of monolayers grown on glass coverslips. Fluorescent labeling of cell F-actin showed that increased F-actin in the perijunctional ring correlated with higher TJ Na permeability. Although a low dose of cytochalasin B did not change TJ Na permeability, it disrupted the cytoskeleton and blocked the decrease in TJ Na permeability caused by glucose. Cytochalasin D failed to block the effects of protein kinase A stimulation or inhibition an TJ Na permeability. We conclude that light junction sodium permeability is regulated both by protein kinase A activity and by other processes involving the actin cytoskeleton.

Original languageEnglish (US)
Pages (from-to)93-104
Number of pages12
JournalJournal of Membrane Biology
Volume161
Issue number1
DOIs
StatePublished - Jan 1 1998
Externally publishedYes

Keywords

  • Cytochalasin D
  • Cytoskeleton
  • Glucose
  • Phalloidin
  • Protein kinase A
  • Sodium permeability
  • Transepithelial electrical resistance

ASJC Scopus subject areas

  • Biophysics
  • Physiology
  • Cell Biology

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