Journal article
TSH regulates pendrin membrane abundance and enhances iodide efflux in thyroid cells
Endocrinology (Philadelphia), Vol.153(1), pp.512-521
01/2012
DOI: 10.1210/en.2011-1548
PMCID: PMC3249672
PMID: 22109890
Abstract
Thyroid hormones are essential for normal development and metabolism. Their synthesis requires transport of iodide into thyroid follicles. The mechanisms involving the apical efflux of iodide into the follicular lumen are poorly elucidated. The discovery of mutations in the SLC26A4 gene in patients with Pendred syndrome (congenital deafness, goiter, and defective iodide organification) suggested a possible role for the encoded protein, pendrin, as an apical iodide transporter. We determined whether TSH regulates pendrin abundance at the plasma membrane and whether this influences iodide efflux. Results of immunoblot and immunofluorescence experiments reveal that TSH and forskolin rapidly increase pendrin abundance at the plasma membrane through the protein kinase A pathway in PCCL-3 rat thyroid cells. The increase in pendrin membrane abundance correlates with a decrease in intracellular iodide as determined by measuring intracellular (125)iodide and can be inhibited by specific blocking of pendrin. Elimination of the putative protein kinase A phosphorylation site T717A results in a diminished translocation to the membrane in response to forskolin. These results demonstrate that pendrin translocates to the membrane in response to TSH and suggest that it may have a physiological role in apical iodide transport and thyroid hormone synthesis.
Details
- Title: Subtitle
- TSH regulates pendrin membrane abundance and enhances iodide efflux in thyroid cells
- Creators
- Liuska Pesce - Division of Endocrinology, Metabolism, and Molecular Medicine, Feinberg School of Medicine, Northwestern University, 303 East Chicago Avenue, Chicago, Illinois 60611, USAAigerim BizhanovaJuan Carlos CaraballoWhitney WestphalMaria L ButtiAlejandro ComellasPeter Kopp
- Resource Type
- Journal article
- Publication Details
- Endocrinology (Philadelphia), Vol.153(1), pp.512-521
- DOI
- 10.1210/en.2011-1548
- PMID
- 22109890
- PMCID
- PMC3249672
- ISSN
- 0013-7227
- eISSN
- 1945-7170
- Grant note
- R01 DK063024 / NIDDK NIH HHS K01 HL080966 / NHLBI NIH HHS 1R01DK63024-01 / NIDDK NIH HHS K01HL080966-01 / NHLBI NIH HHS
- Language
- English
- Date published
- 01/2012
- Academic Unit
- Pulmonary, Critical Care, and Occupational Medicine; Endocrinology and Diabetes; ICTS; Stead Family Department of Pediatrics; Internal Medicine
- Record Identifier
- 9984093603002771
Metrics
21 Record Views