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Regulated transport of sulfate and oxalate by SLC26A2/DTDST

John F Heneghan1, Arash Akhavein, Maria J Salas

  • 1Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.

American Journal of Physiology. Cell Physiology
|March 12, 2010
PubMed

Insights

The SLC26A2 transporter facilitates oxalate and sulfate transport in the intestine, impacting nephrolithiasis. This study characterizes SLC26A2

Area of Science:

  • Molecular biology
  • Physiology
  • Nephrology

Background:

  • Nephrolithiasis is associated with reduced intestinal oxalate secretion in Slc26a6(-/-) mice.
  • The specific enterocyte pathways for oxalate absorption and Slc26a6-independent secretion remain unclear.
  • Intestinal expression of the sulfate transporter SLC26A2 suggests a potential role in anion transport.

Purpose of the Study:

  • To investigate the transport of oxalate and other anions by human SLC26A2 and mouse Slc26a2.
  • To characterize the kinetic properties and regulatory mechanisms of SLC26A2-mediated transport.

Main Methods:

  • Expression of human SLC26A2 and mouse Slc26a2 in Xenopus oocytes.
  • Measurement of radiolabeled oxalate, sulfate, and chloride uptake and exchange.
  • Assessment of transport inhibition by varying substrate concentrations, pH, and protein kinase C activity.
  • Analysis of transport in diastrophic dysplasia mutants of SLC26A2.

Main Results:

  • SLC26A2 mediates saturable uptake of oxalate with cis-inhibition by sulfate.
  • SLC26A2 facilitates bidirectional exchange of oxalate/sulfate and sulfate/chloride, which is not detectably electrogenic.
  • Extracellular chloride dependence was observed for efflux, and acidic extracellular pH inhibited all SLC26A2-mediated exchanges.
  • Acidic intracellular pH selectively activated chloride/sulfate exchange, and protein kinase C inhibited SLC26A2 by reducing surface abundance.
  • Diastrophic dysplasia mutants showed reduced uptake of sulfate and oxalate, with altered surface abundance.

Conclusions:

  • SLC26A2 functions as a key transporter of oxalate and sulfate in the intestine.
  • SLC26A2 plays a role in Slc26a6-independent intestinal oxalate secretion.
  • Understanding SLC26A2 transport mechanisms and regulation is crucial for managing nephrolithiasis.

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