Dossena Silvia, Maccagni Antonella, Vezzoli Valeria, Bazzini Claudia, Garavaglia Maria Lisa, Meyer Giuliano, Fürst Johannes, Ritter Markus, Fugazzola Laura, Persani Luca, Zorowka Patrick, Storelli Carlo, Beck-Peccoz Paolo, Bottà Guido, Paulmichl Markus
Department of Biomolecular Sciences and Biotechnology, Università degli Studi di Milano,Via Celoria 26, I-20133 Milan, Italy.
Eur J Endocrinol. 2005 Nov;153(5):693-9. doi: 10.1530/eje.1.02018.
The SLC26A4 protein (pendrin) seems to be involved in the exchange of chloride with other anions, therefore being responsible for iodide organification in the thyroid gland and the conditioning of the endolymphatic fluid in the inner ear. Malfunction of SLC26A4 leads to Pendred syndrome, characterized by mild thyroid dysfunction often associated with goiter and/or prelingual deafness. The precise function of the SLC26A4 protein, however, is still elusive. An open question is still whether the SLC26A4-induced ion exchange mechanism is electrogenic or electroneutral. Recently, it has been shown that human pendrin expressed in monkey cells leads to chloride currents.
We overexpressed the human SLC26A4 isoform in HEK293 Phoenix cells and measured cationic and anionic currents by the patch-clamp technique in whole cell configuration.
Here we show that human pendrin expressed in human cells does not lead to the activation of chloride currents, but, in contrast, leads to an increase of cationic currents.
Our experiments suggest that the SLC26A4-induced chloride transport is electroneutral when expressed in human cellular systems.
SLC26A4蛋白（pendrin）似乎参与氯离子与其他阴离子的交换，因此负责甲状腺中的碘有机化以及内耳内淋巴液的调节。SLC26A4功能异常会导致 Pendred 综合征，其特征为常伴有甲状腺肿和/或语前聋的轻度甲状腺功能障碍。然而，SLC26A4蛋白的确切功能仍不清楚。一个悬而未决的问题仍然是SLC26A4诱导的离子交换机制是生电的还是电中性的。最近，研究表明在猴细胞中表达的人pendrin会导致氯离子电流。
我们在HEK293 Phoenix细胞中过表达人SLC26A4异构体，并通过膜片钳技术在全细胞模式下测量阳离子和阴离子电流。
我们在此表明，在人细胞中表达的人pendrin不会导致氯离子电流的激活，相反，会导致阳离子电流增加。
我们的实验表明，当在人细胞系统中表达时，SLC26A4诱导的氯离子转运是电中性的。
