Abstract
The parathyroid hormone (PTH) gene consists of three exons. The parathyroid glands develop from a shared initial organ primordium together with the thymus. 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) decreases PTH gene transcription. The major regulator of the parathyroid is hypocalcemia. Hypocalcemia regulates PTH gene expression in vivo by increasing PTH mRNA levels, and this is mainly posttranscriptional. Phosphate also independently regulates PTH gene expression. The effects of phosphate and uremia are also posttranscriptional. Trans-acting parathyroid cytosolic proteins bind to a defined cis element in the PTH mRNA 3′ UTR. This binding determines the degradation of PTH mRNA and thereby the PTH mRNA half-life. Pin1 regulates protein–PTH mRNA interactions leading to more rapid PTH mRNA decay. Fibroblast growth factor 23 (FGF23) acts on its receptor, the klotho–FGFR1c receptor, to decrease PTH mRNA levels and secretion. In advanced chronic kidney disease there is resistance of the parathyroid to the high FGF23 levels due to downregulation of the FGF23 receptor.
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