Regulation of the MDCK Cell Tight Junction |
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Authors: | ON Kovbasnjuk U Szmulowicz KR Spring |
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Institution: | (1) Laboratory of Kidney and Electrolyte Metabolism, National Heart Lung and Blood Institute, National Institutes of Health, Building 10, Room 6N260, Bethesda, MD 20892-1603, USA, US |
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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 D 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
on TJ Na permeability. We conclude that tight junction sodium permeability is regulated both by protein kinase A activity
and by other processes involving the actin cytoskeleton.
Received: 17 June 1997/Revised: 28 August 1997 |
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Keywords: | : Glucose — Protein kinase A — Cytoskeleton — Sodium permeability — Transepithelial electrical resistance — Phalloidin — Cytochalasin D |
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