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© 1990 Oxford University Press

research-article

The effects of teleocidin and aplysiatoxin tumor promoters on epithelial tight junctions and transepithelial permeability: comparison to phorbol esters

James M. Mullin 1, Mary T. McGinn, Kathleen V. Snock and Shotaro Imaizumi 2

The Lankenau Medical Research Center Lancaster Avenue West of City Line, Philadelphia, PA 19151, USA
2Department of Pathology, Lankenau Hospital Lancaster Avenue West of City Line, Philadelphia, PA 19151, USA

1To whom reprint requests should be Sent

Control of transepithelial permeability by regulation of tight junctions is exerted by the non-phorbol ester tumor promoters, teleocidin and aplysiatoxin. Similar to the phorbol esters, tetradecanoylphorbol-13-acetate (TPA) and phorbol dibutyrate (PDBU), both teleocidin and aplysiatoxin cause a reversible decrease of transepithelial voltage and transepithelial resistance across LLC-PK1 renal epithelial cell sheets at concentrations as low as 10-8M. These compounds are effective from either side of these polar epithelial cells, i.e. apical or basolateral. The decreases in transepithelial gradients and resistance are paralleled by a rise in the transepithelial (paracellular) flux of D-mannitol between the cells (through the tight junctions). These four tumor promoters, TPA, PDBU, teleocidin and aplysiatoxin, are all known protein kinase C activators, and support the case for proteinkinase-C-mediated control of tight junctional permeability.


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