Vitamin D3 upregulates plasma membrane Ca2+-ATPase expression and potentiates apico-basal Ca2+ flux in MDCK cells

Sertac N. Kip, Emanuel E. Strehler

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Plasma membrane Ca2+-ATPases (PMCAs) are a ubiquitous system for the expulsion of Ca2+ from eukaryotic cells. In tight monolayers of polarized Madin-Darby canine kidney (MDCK) cells representing a distal kidney tubule model, PMCAs are responsible for about one-third of the vectorial Ca2+ transport under resting conditions, with the remainder being provided by the Na+/ Ca2+ exchanger. Vitamin D 3 (VitD) is known to increase PMCA expression and activity in Ca 2+-transporting tissues such as the intestine, as well as in osteoblasts and Madin-Darby bovine kidney epithelial cells. We found that VitD upregulated the expression of the PMCAs (mainly PMCA4b) in MDCK cell lysates at the RNA and protein level in a time- and dose-dependent manner. Interestingly, VitD caused a decrease of the PMCAs in the apical plasma membrane fraction and a concomitant increase of the pumps in the basolateral membrane. Functional studies demonstrated that transcellular 45Ca2+ flux from the apical-to-basolateral compartment was significantly enhanced by VitD. These findings demonstrate that VitD is a positive regulator of the PMCAs in MDCK epithelial cells. The correlation of decreased apical/increased basolateral expression of the PMCAs with an increase in transcellular Ca2+ flux from the apical (urine) toward the basolateral (blood) compartment indicates the physiological relevance of VitD function in kidney tubular Ca2+ reabsorption.

Original languageEnglish (US)
Pages (from-to)F363-F369
JournalAmerican Journal of Physiology - Renal Physiology
Issue number2 55-2
StatePublished - Feb 2004


  • Calcium transport
  • Kidney distal tubule
  • Madin-Darby canine kidney
  • Transcellular ion flux

ASJC Scopus subject areas

  • Physiology
  • Urology


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