Controversies concerning the role of pendrin as an apical iodide transporter in thyroid follicular cells

Aigerim Bizhanova*, Peter Kopp

*Corresponding author for this work

Research output: Contribution to journalReview article

33 Scopus citations

Abstract

Pendred syndrome is an autosomal recessive disorder defined by sensorineural deafness, goiter and a partial organification defect of iodide. It is caused by biallelic mutations in the multifunctional anion transporter pendrin/SLC26A4. In human thyroid tissue, pendrin is localized at the apical membrane of thyroid follicular cells. The clinical phenotype of patients with Pendred syndrome and the fact that pendrin can mediate iodide efflux in transfected cells suggest that this anion exchanger may be involved in mediating iodide efflux into the follicular lumen, a key step in thyroid hormone biosynthesis. This concept has, however, been questioned. This review discusses supporting evidence as well as arguments questioning a role of pendrin in mediating iodide efflux in thyrocytes.

Original languageEnglish (US)
Pages (from-to)485-490
Number of pages6
JournalCellular Physiology and Biochemistry
Volume28
Issue number3
DOIs
StatePublished - 2011

Keywords

  • Goiter
  • Hypothyroidism
  • Pendred syndrome
  • Pendrin
  • SLC26A4
  • Thyroid hormone synthesis

ASJC Scopus subject areas

  • Physiology

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