title: Contraction of epithelial (MDCK) cells in response to low extracellular calcium is dependent on extracellular sodium.
abstract: Like other cells of epithelial origin, MDCK cells respond with a reversible structural transformation to a diminution in the concentration of extracellular Ca2+. Upon deprivation of Ca2+ in the medium the cells undergo an active contraction mediated by the actin-myosin cytoskeleton, in parallel to detachment of the intercellular contacts and appearance of free spaces in the epithelium or monolayer (Castillo et al., 1998). We now present results indicating that the decrease of external Ca2+ plays an indirect and non-specific role in activating contraction, probably by allowing an influx of Na+. The omission of external Ca2+ had no effect when it was replaced by Mg2+, Ba2+ or Hg2+, and the addition of any of these divalent cations induced relaxation of cells previously contracted by exposure to low Ca2+. A null or weak response was observed also when Ca2+ was lowered in a solution where Na+ was replaced by choline or in the presence of amiloride (30 microM), which reduces the permeability of the plasma membrane to Na+. Restitution of Na+ or removal of amiloride were followed by contraction in the same cultures. Li+ proved an able substitute of Na+ as requisite for cell contraction in response to Ca2+ depletion. Monensin (0.1 mM) -an ionophore selective for Na+- and to a lesser extent ouabain (0.1 mM) -an inhibitor of Na+ extrusion across the plasma membrane- , both stimulated contraction in the presence of the normal level of external Ca2+. Decreasing by half the normal concentration of external K+ facilitated cell contraction, but typical responses were observed when K+ was increased to 40 mM by partial substitution for Na+. These findings attest that cell contraction in response to low Ca2+ is likely due to an increase in the permeability of the plasma membrane to Na+, though not to membrane depolarization as such. Evidences from other motile systems suggest that Na+ influx might in turn cause an elevation of cytoplasmic Ca2+, which activates the actin-myosin cytoskeleton.
authors.affiliation: Departamento de Biologia Celular, Centro de Investigación y de Estudios Avanzados del IPN, México, DF.
authors.forename: R
authors.initials: R
authors.lastname: Lagunes
authors.forename: L
authors.initials: L
authors.lastname: Ruiz
authors.forename: E
authors.initials: E
authors.lastname: Frixione
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002118:Calcium / Q000172:deficiency / Q000494:pharmacology*; D002460:Cell Line; D048429:Cell Size / Q000187:drug effects; D004847:Epithelial Cells / Q000187:drug effects*; D008094:Lithium / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D008628:Mercury / Q000494:pharmacology; D008858:Microscopy, Phase-Contrast; D008985:Monensin / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology*
chemical_list: D001464:Barium; D010042:Ouabain; D000584:Amiloride; D008985:Monensin; D008094:Lithium; D012964:Sodium; D008628:Mercury; D008274:Magnesium; D011188:Potassium; D002118:Calcium