SLC26A4 expression among autoimmune thyroid tissues

ContextThe PDS gene (SLC26A4) is responsible for Pendred syndrome (PS). Genetic analysis of PDS using Tunisian samples showed evidence for linkage and association with autoimmune thyroid diseases (AITD) emergence. In addition, the PDS gene product, pendrin, was recently identified as a novel autoantigen in Graves’ disease (GD) or Hashimoto thyroiditis (HT) patients’ sera.ObjectiveThe aim of this study was to quantify the PDS gene expression and to evaluate the pendrin in vivo and in vitro immunolocalisation.PatientsA total of 52 thyroid gland tissue samples (22 GD, 11 HT, 5 multinodular goiter (MNG), 3 normal thyroid tissues, 8 papillary thyroid carcinoma (PTC), 1 follicular thyroid carcinoma (FTC) and 2 medullar thyroid carcinoma (MTC)) were explored.Method PDS and pendrin expression levels were determined using quantitative RT-PCR and immuno-detection methods. TSH and thyroglobulin (Tg) effects on pendrin expression were investigated by immunofluorescence on primary cell culture from GD thyroid tissues.ResultsThe relative quantification using PDS transcript level among GD thyroid tissues was increased compared to normal thyroid tissues used as calibrator (mean: 27.17-fold higher than normal thyroid tissues). However, thyroids with HT, carcinoma and MNG showed a decrease expression level (means: 92.05-, 77.68-, 14.3-fold lower than normal thyroid tissues, respectively). These results were confirmed by immunoanalysis. Immunofluorescence results showed an apical and a cytoplasmic pendrin localisation on GD thyroid tissues and a marked pendrin expression reduction on HT thyroid tissues. GD primary cell cultures under TSH and Tg stimulation showed a trafficking improvement of pendrin apical localisation.ConclusionsOur data point to the presence of a relation between SLC26A4 expression in AITD and thyroid function.