Hormonal regulation of cell junction permeability: upregulation by catecholamine and prostaglandin E1.
By cellular activation with hormones, we test the proposition (Loewenstein, W.R., Physiol. Rev. 61:829, 1981) that the permeability of cell junction is upregulated through elevation of the level of cyclic AMP. Cultured rat glioma C-6 cells, with beta-adrenergic receptors, and human lung WI-38 cells, with prostaglandin receptors, were exposed to catecholamine (isoproterenol) and prostaglandin E1, respectively, while their junctions were probed with microinjected fluorescent-labelled mono-, di-, and triglutamate. Junctional permeability, as indexed by the proportion of cell interfaces transferring the probes, rose after the hormones treatments. The increase in permeability took several hours to develop and was associated with an increase in the number of gap-junctional membrane with an increase in the number of gap-junctional membrane particles (freeze-fracture electron microscopy). Such interaction between hormonal and junctional intercellular communication may provide a mechanism for physiological regulation of junctional communication and (perhaps as part of that) for physiological coordination of responses of cells in organ and tissues to hormones.
D000527:Alprostadil; D000818:Animals; D002450:Cell Communication / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects*; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism / Q000494:pharmacology; D005910:Glioma / Q000378:metabolism; D006801:Humans; D007365:Intercellular Junctions / Q000187:drug effects* / Q000378:metabolism; D007545:Isoproterenol / Q000494:pharmacology*; D008168:Lung / Q000378:metabolism; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats
D011458:Prostaglandins E; D000242:Cyclic AMP; D000527:Alprostadil; D007545:Isoproterenol