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The making of a tight junction
M Cereijido1, L González-Mariscal, R G Contreras
1Center for Research and Advanced Studies, México, DF, México.
Journal of Cell Science. Supplement
|January 1, 1993
Summary
Calcium (Ca2+) is crucial for forming tight junctions (TJs) in dog kidney epithelial cells. Its presence accelerates TJ formation and influences epithelial electrical resistance.
Area of Science:
- Cell Biology
- Epithelial Biology
- Biochemistry
Background:
- Madin-Darby Canine Kidney (MDCK) cells form tight junctions (TJs) when confluent.
- TJ formation is a complex process requiring protein synthesis, actin cytoskeleton organization, and calcium (Ca2+).
Purpose of the Study:
- To investigate the role of Ca2+ in the kinetics and mechanisms of TJ formation in MDCK cells.
- To understand how extracellular factors modulate TJ formation and epithelial electrical resistance.
Main Methods:
- Culturing MDCK cells to confluence.
- Inducing TJ formation with and without Ca2+.
- Measuring transepithelial electrical resistance (TER).
Main Results:
- TJ formation in MDCK cells requires Ca2+ and takes 12-15 hours.
- Absence of Ca2+ prevents TJ formation, but its subsequent addition accelerates it.
- Ca2+ acts extracellularly, activating uvomorulin and downstream signaling pathways (G-proteins, phospholipase C, protein kinase C).
- Epithelial TER is modulated by various agents, serum, and urine components.
Conclusions:
- Ca2+ is essential for initiating TJ assembly in epithelial cells.
- The extracellular Ca2+ binding site on uvomorulin is critical for TJ formation.
- Modulation of TJ formation by external agents can significantly alter epithelial barrier function (TER).