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• W2080684005 endingPage "1449" @default.
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• W2080684005 abstract "Resistance to the action of parathyroid hormone (PTH) has been demonstrated in end-stage renal failure and is considered to be important in the pathogenesis of secondary hyperparathyroidism. The mechanism of resistance is unknown. However, altered regulation of cellular PTH/PTH-related protein (PTH/PTHrP) receptor (PTH1R) has been assumed to be important.We have used in situ hybridization to examine PTH1R mRNA expression by osteoblasts in human bone and have compared the expression in high- and low-turnover renal bone disease, high-turnover nonrenal bone disease (healing fracture callus and Pagetic bone), and normal bone. Bone biopsies were formalin fixed, ethylenediaminetetraacetic acid decalcified, and paraffin wax embedded. A 1.8 kb PTH1R cDNA probe, labeled with 35S, was used, and the hybridization signal was revealed by autoradiography. The density of signal over osteoblasts was quantitated using a semiautomated Leica image analysis software package.The mean density of PTH1R mRNA signal over osteoblasts in renal high-turnover bone was only 36% of that found in nonrenal high-turnover bone (P < 0.05) and 51% of that found in normal bone (P < 0.05). Osteoblast PTH1R mRNA signal in adynamic bone from individuals with diabetes mellitus was 28% of normal bone (P < 0.05) and 54% of that found in renal high-turnover bone (P < 0.05).These results demonstrate a down-regulation of osteoblast PTH1R mRNA in end-stage renal failure in comparison to normal and high-turnover bone from otherwise healthy individuals, and provide an insight into the mechanisms of skeletal resistance to the actions of PTH." @default.
• W2080684005 created "2016-06-24" @default.
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• W2080684005 date "2000-10-01" @default.
• W2080684005 modified "2023-10-15" @default.
• W2080684005 title "Down-regulation of human osteoblast PTH/PTHrP receptor mRNA in end-stage renal failure" @default.
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• W2080684005 doi "https://doi.org/10.1046/j.1523-1755.2000.00306.x" @default.
• W2080684005 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11012879" @default.
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