ArticleThe Journal of membrane biology2010
Epithelial barrier resistance is increased by the divalent cation zinc in cultured MDCKII epithelial monolayers.
Article in The Journal of membrane biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 15 citations in OpenAlex.
- Micronutrient Improvement of Epithelial Barrier Function in Various Disease States: A Case for Adjuvant Therapy.International journal of molecular sciences · 2022Review
- Remodeling of Tight Junctions and Enhancement of Barrier Integrity of the CACO-2 Intestinal Epithelial Cell Layer by Micronutrients.PloS one · 2015Article
- Zinc and gastrointestinal disease.World journal of gastrointestinal pathophysiology · 2014Review
- Zinc supplementation modifies tight junctions and alters barrier function of CACO-2 human intestinal epithelial layers.Digestive diseases and sciences · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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 (P(Na)/P(Cl) from 4.9 to 2.3 and P(Na)/P(choline) 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.
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Registered trials
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