Abstract
In primary hyperparathyroidism, chronically elevated levels of PTH produce low serum phosphorus through inhibition of proximal tubule expression of sodium‐phosphate cotransporters. We have previously shown that chronic PTH stimulation of proximal tubule cells is associated with decreased expression of NpT2a mRNA through destabilization, which is dependent on transcription. BLAST evaluation of the NpT2a promoter identified a CREB‐binding region. We hypothesize that PTH decreases NpT2a mRNA stability through activation of the PKA pathway. Opossum kidney (OK) cells were transfected with luciferase reporter gene constructs containing either full‐length or serially truncated NpT2a promoter regions. Luciferase reporter assays show no effect of PTH on the promoter function of the NpT2a gene. Direct activation of PKA with 8Br‐cAMP and PKC with PMA for 2h produced a decrease in NpT2a mRNA of 35.6 ± 12.2% and 28.9 ± 4.3%, respectively. We conclude that PTH decreases NpT2a mRNA expression through destabilization of NpT2a mRNA, and that both PKA and PKC pathways may contribute to this effect. Support for this project is provided by VA to EDL.
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