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Coordinated control of renal Ca(2+) transport proteins by parathyroid hormone van Abel M; Hoenderop JG; van der Kemp AW; Friedlaender MM; van Leeuwen JP; Bindels RJKidney Int 2005[Oct]; 68 (4): 1708-21BACKGROUND: The kidney is one of the affected organs involved in the clinical symptoms of parathyroid hormone (PTH)-related disorders, like primary hyperparathyroidism and familial hypocalciuric hypercalcemia. The molecular mechanism(s) underlying alterations in renal Ca(2+) handling in these disorders is poorly understood. METHODS: Parathyroidectomized and PTH-supplemented rats and mice infused with the calcimimetic compound NPS R-467 were used to study the in vivo effect of PTH on the expression of renal transcellular Ca(2+) transport proteins, including the epithelial Ca(2+) channel transient receptor potential, vanilloid, member 5 (TRPV5), calbindins, and the Na(+)/Ca(2+)-exchanger (NCX1). In addition, the effect of PTH on transepithelial Ca(2+) transport in rabbit connecting tubule/cortical collecting duct (CNT/CCD) primary cultures was determined. RESULTS: Decreased PTH levels in parathyroidectomized rats or NPS R-467-infused mice, resulted in reduced expression of these proteins, which is consistent with diminished Ca(2+) reabsorption, causing the development of the observed hypocalcemia. PTH supplementation of parathyroidectomized rats restored the expression of the renal Ca(2+) transport machinery and serum Ca(2+) levels, independent of serum 1,25-dihydroxyvitamin D(3) levels and renal vitamin D or Ca(2+)-sensing receptor mRNA abundance. Inhibition of the PTH-stimulated transepithelial Ca(2+) transport by the TRPV5-specific inhibitor ruthenium red reduced the PTH-stimulated expression of calbindin-D(28K) and NCX1 in rabbit CNT/CCD primary cultures. CONCLUSION: PTH stimulates renal Ca(2+) reabsorption through the coordinated expression of renal transcellular Ca(2+) transport proteins. Moreover, the PTH-induced stimulation is enhanced by the magnitude of the Ca(2+) influx through the gatekeeper TRPV5, which in turn facilitates the expression of the downstream Ca(2+) transport proteins. Therefore, the renal transcellular Ca(2+) transport proteins, including TRPV5, could contribute to the pathogenesis of PTH-related disorders.|Aniline Compounds/pharmacology[MESH]|Animals[MESH]|Calbindins[MESH]|Calcium Channels/genetics/*metabolism[MESH]|Calcium/agonists/*metabolism[MESH]|Cells, Cultured[MESH]|Epithelial Cells/cytology/drug effects/metabolism[MESH]|Gene Expression[MESH]|Hypocalcemia/drug therapy/metabolism/physiopathology[MESH]|Kidney/cytology/*physiology[MESH]|Male[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Parathyroid Hormone/blood/pharmacology/*physiology[MESH]|Parathyroidectomy[MESH]|Rabbits[MESH]|Rats[MESH]|Rats, Inbred Strains[MESH]|Receptors, Calcium-Sensing/genetics/metabolism[MESH]|S100 Calcium Binding Protein G/genetics/metabolism[MESH]|Sodium-Calcium Exchanger/genetics/metabolism[MESH]|TRPV Cation Channels/genetics/*metabolism[MESH] |
