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SLC26A6 and NaDC-1 transporters interact to regulate oxalate and citrate homeostasis

Ehud Ohana1, Nikolay Shcheynikov, Orson W Moe

  • 1Epithelial Signaling and Transport Section, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, and.

Journal of the American Society of Nephrology : JASN
|July 9, 2013
PubMed

Insights

The oxalate transporter SLC26A6 and citrate transporter NaDC-1 interact to regulate urinary oxalate and citrate levels. This interaction may be key in preventing calcium oxalate stone formation.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Biochemistry

Background:

  • Hyperoxaluria and hypocitraturia contribute to calcium oxalate stone formation.
  • The precise molecular mechanisms governing urinary oxalate and citrate levels remain incompletely understood.

Purpose of the Study:

  • To investigate the interplay between the oxalate transporter SLC26A6 and the citrate transporter NaDC-1.
  • To elucidate their roles in maintaining citrate and oxalate homeostasis.

Main Methods:

  • Utilized Slc26a6-null mice to assess renal and intestinal transport.
  • Employed Xenopus oocyte co-expression systems to study transporter interactions.
  • Conducted biochemical and physiological analyses to identify interaction domains.

Main Results:

  • Slc26a6-null mice showed increased sodium-dependent succinate uptake, hyperoxaluria, and hypocitraturia, suggesting enhanced NaDC-1 activity.
  • Co-expression studies revealed that NaDC-1 enhances SLC26A6 activity, while SLC26A6 inhibits NaDC-1 activity, restricting citrate reabsorption.
  • The STAS domain of SLC26A6 and the first intracellular loop of NaDC-1 were identified as crucial for their interaction.

Conclusions:

  • A molecular pathway involving SLC26A6 and NaDC-1 tightly regulates oxalate and citrate levels.
  • This interaction pathway is a potential determinant of calcium oxalate stone formation.

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