Lack of Na+,K+-ATPase expression in intercalated cells may be compensated by Na+-ATPase: A study on MDCK – C11 cells

Abstract

The lack of Na(+),K(+)-ATPase expression in intercalated cells (IC) is an intriguing condition due to its fundamental role in cellular homeostasis. In order to better understand this question we compared the activities of Na(+),K(+)-ATPase and Na(+)-ATPase in two MDCK cell clones: the C11, with IC characteristics, and the C7, with principal cells (PC) characteristics. The Na(+),K(+)-ATPase activity found in C11 cells is far lower than in C7 cells and the expression of its beta-subunit is similar in both cells. On the other hand, a subset of C11 without alpha-subunit expression has been found. In C11 cells the Na(+)-ATPase activity is higher than that of the Na(+),K(+)-ATPase, and it is increased by medium alkalinization, suggesting that it could account for the cellular Na(+)-homeostasis. Although further studies are necessary for a better understanding of these findings, the presence of Na(+)-ATPase may explain the adequate survival of cells that lack Na(+),K(+)-ATPase.

Recent advances in distal tubular potassium handling

“…One possibility is through the ouabain-insensitive Na-ATPase. In a recent study, this activity was observed in intercalated cell-like MDCK C11 cells at levels similar to those seen for the ouabain-sensitive Na-K-ATPase found in principal cell-like MDCK C7 cells (58). The molecular identity of this ATPase is unknown.…”

Role of NKCC in BK channel-mediated net K+secretion in the CCD

“…Na ϩ -ATPase V max is increased by addition of micromolar concentrations of Ca 2ϩ to the assay medium (51) while the Na ϩ -K ϩ -ATPase is inhibited by this concentration of Ca 2ϩ (9). Madin-Darby canine kidney (MDCK) C11 cells, the majority of which possess ␤-intercalated cell characteristics (including peanut lectin agglutin binding), exhibit significantly greater Na ϩ -ATPase activity and far lower Na ϩ -K ϩ -ATPase activity than that measured in C7 principal-like MDCK cells (58).…”