Epithelial Barrier Resistance is Increased by the Divalent Cation Zinc in Cultured MDCKII Epithelial Monolayers

Epithelial Barrier Resistance is Increased by the Divalent Cation Zinc in Cultured MDCKII... Topical zinc applications promote wound healing and epithelialization. “Leaky” MDCKII epithelia exposed to apical ZnCl2 (10 mM) showed a time-dependent increase (t 0.5 22.2 ± 2.7 min) of transepithelial resistance (R t) from 82.3 ± 2.4 Ω cm2 to 1,551 ± 225.6 Ω cm2; the increase was dose-dependent, being observed at 3 mM but not at 1 mM. Basal Zn2+ applications also increased epithelial resistance (at 10 mM to 323 ± 225.6 Ω cm2). The linear current–voltage relationship in control epithelia changed after apical 10 mM ZnCl2 to show rectification. Voltage deflections resulting from inward currents showed time-dependent relaxation (basal potential difference (p.d.)-positive), with outward currents being time-independent. Cation selectivity was tested after apical ZnCl2 elevated resistance; both the NaCl:mannitol (basal replacement) dilution p.d. and the choline:Na bi-ionic p.d. decreased (PNa/PCl from 4.9 to 2.3 and PNa/Pcholine from 3.8 to 2.1, respectively). Transepithelial paracellular basal to apical 45Ca fluxes increased approximately twofold when driven by a basal positive Na:NMDG bi-ionic p.d., but with basal 10 mM ZnCl2, 45Ca fluxes decreased approximately twofold. Neither ZO-1 nor occludin distribution was altered after ~2-h exposure to apical 10 mM ZnCl2. However, claudin-2, though present at the tight junction, increased within the cell. Increased epithelial barrier resistance by Zn2+ is due to modification of the paracellular pathway, most probably by multiple mechanisms. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Epithelial Barrier Resistance is Increased by the Divalent Cation Zinc in Cultured MDCKII Epithelial Monolayers

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Publisher
Springer-Verlag
Copyright
Copyright © 2010 by Springer Science+Business Media, LLC
Subject
Life Sciences; Human Physiology ; Biochemistry, general
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s00232-010-9312-z
Publisher site
See Article on Publisher Site

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