Proximal Tubular Phosphate Reabsorption: Molecular Mechanisms

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Abstract
Renal proximal tubular reabsorption of Piis a key element in overall Pihomeostasis, and it involves a secondary active Pitransport mechanism. Among the molecularly identified sodium-phosphate (Na/Pi) cotransport systems a brush-border membrane type IIa Na-Picotransporter is the key player in proximal tubular Pireabsorption. Physiological and pathophysiological alterations in renal Pireabsorption are related to altered brush-border membrane expression/content of the type IIa Na-Picotransporter. Complex membrane retrieval/insertion mechanisms are involved in modulating transporter content in the brush-border membrane. In a tissue culture model (OK cells) expressing intrinsically the type IIa Na-Picotransporter, the cellular cascades involved in “physiological/pathophysiological” control of Pireabsorption have been explored. As this cell model offers a “proximal tubular” environment, it is useful for characterization (in heterologous expression studies) of the cellular/molecular requirements for transport regulation. Finally, the oocyte expression system has permitted a thorough characterization of the transport characteristics and of structure/function relationships. Thus the cloning of the type IIa Na-Picotransporter (in 1993) provided the tools to study renal brush-border membrane Na-Picotransport function/regulation at the cellular/molecular level as well as at the organ level and led to an understanding of cellular mechanisms involved in control of proximal tubular Pihandling and, thus, of overall Pihomeostasis.

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