Nickel-induced increases in gap junctional communication in the uterine cell line SK-UT-1

• Published in: In vitro cellular & developmental biology Vol. 29A; no. 3 Pt 1; p. 215
• Main Authors: Marty, M S, Loch-Caruso, R
• Format: Journal Article
• Language: English
• Published: United States 01.03.1993
• Subjects: Cell Communication - drug effects; Cell Line - drug effects; Cell Line - metabolism; Dose-Response Relationship, Drug; Female; Humans; Intercellular Junctions - drug effects; Isoquinolines; Magnesium Sulfate - pharmacology; Nickel - antagonists & inhibitors; Nickel - pharmacology; Time Factors; Uterine Contraction
• ISSN: 0883-8364
• DOI: 10.1007/BF02634186

Previous studies have suggested that gap junctions may have a role in various uterine functions, including parturition. Because nickel has been demonstrated to increase uterine contractility in vitro, the effect of nickel (II) chloride on gap junctional communication was assessed in a tumorigenic uterine cell line, SK-UT-1 (ATCC HTB 114). Cells were exposed in vitro to 25 and 50 microM NiCl2 for 24 h or 100 microM NiCl2 for 3, 12, and 24 h, then functional gap junctional communication was measured as the transfer of Lucifer yellow dye from microinjected donor cells to their primary neighbor cells. Dye transfer was significantly increased only in cell cultures exposed to 100 microM NiCl2 for 24 h, compared to untreated controls, lower doses, and shorter exposure periods. This response was inhibited by the simultaneous co-treatment of SK-UT-1 cells with magnesium by adding 100 microM MgSO4 to the dosing medium. Possible mechanisms and implications for these findings are discussed.