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CFTR–SLC26 transporter interactions in epithelia

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Abstract

Transport mechanisms that mediate the movements of anions must be coordinated tightly in order to respond appropriately to physiological stimuli. This process is of paramount importance in the function of diverse epithelial tissues of the body, such as, for example, the exocrine pancreatic duct and the airway epithelia. Disruption of any of the finely tuned components underlying the transport of anions such as Cl−, HCO3 −, SCN−, and I− may contribute to a plethora of disease conditions. In many anion-secreting epithelia, the interactions between the cystic fibrosis transmembrane conductance regulator (CFTR) and solute carrier family 26 (SLC26) transporters determine the final exit of anions across the apical membrane and into the luminal compartment. The molecular identification of CFTR and many SLC26 members has enabled the acquisition of progressively more detailed structural information about these transport molecules. Studies employing a vast array of increasingly sophisticated approaches have culminated in a current working model which places these key players within an interactive complex, thereby setting the stage for future work.

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Notes

  1. HCO3 − is appreciated as an important buffer of not only the intracellular milieu, but also of fluid secretions. Thyroid hormone synthesis requires the incorporation, and hence the transport of I−. SCN− secretion by airway epithelia is necessary for the generation of OSCN− by interaction with peroxidase-generated H2O2. OSCN− has potent anti-microbial action, thereby playing a critical role in innate host airway defense.

  2. DTDST is characterized by skeletal malformations, underscoring the role of SLC26A2 in transporting the substrate (SO4 -2) necessary for the sulfation of cartilage proteoglycans.

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Acknowledgments

Research in the Fong lab is currently funded by the National Institutes of Health (COBRE NIH-P20-RR017686; Project 2) from the IDEA Program of the National Center for Research Resources, as well as an Innovative Research Award from the Kansas State University/Johnson Center for Basic Cancer Research (RFEES1). The contents of this work are solely the responsibility of the author and do not necessarily represent the official views of the Center of Biomedical Research Excellence for Epithelial Function in Health and Disease or NIH.

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  1. Department of Anatomy and Physiology, Kansas State University College of Veterinary Medicine, 1600 Denison Avenue, Manhattan, KS, 66506, USA

    Peying Fong

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Fong, P. CFTR–SLC26 transporter interactions in epithelia. Biophys Rev 4, 107–116 (2012). https://doi.org/10.1007/s12551-012-0068-9

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