{"doi":"10.1073/pnas.0501312102","title":"Parathyroid hormone decreases renal vitamin D receptor expression\n                    <i>in vivo</i>","abstract":"<jats:p>\n                    The vitamin D receptor (VDR) is a nuclear transcription factor responsible for mediating the biological activities of 1,25-dihydroxyvitamin D\n                    <jats:sub>3</jats:sub>\n                    [1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    ]. Renal and parathyroid gland VDR content is an important factor in calcium homeostasis, vitamin D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy. In these tissues, VDR expression is highly regulated by the calcium and vitamin D status. Although 1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastically reduced expression of the receptor. The generation of 25-hydroxyvitamin D\n                    <jats:sub>3</jats:sub>\n                    -1α-hydroxylase-null mice, which are incapable of endogenously producing 1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    , has allowed us to investigate the influence of parathyroid hormone (PTH) on VDR expression independent of PTH-mediated increases in 1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    . Administration of human PTH (1-34) (110 μg/kg per day) for 48 h reduced renal VDR levels from 515 to 435 fmol/mg protein (15%,\n                    <jats:italic>P</jats:italic>\n                    &lt; 0.03) in wild-type mice. In the 25-hydroxyvitamin D\n                    <jats:sub>3</jats:sub>\n                    -1α-hydroxylase-null mice, PTH administration strongly reduced renal VDR levels, from 555 to 394 fmol/mg protein (29%,\n                    <jats:italic>P</jats:italic>\n                    &lt; 0.001). These results demonstrate that PTH is a potent down-regulator of VDR expression\n                    <jats:italic>in vivo</jats:italic>\n                    .\n                  </jats:p>","journal":"Proceedings of the National Academy of Sciences","year":2005,"id":668176,"datarank":0.5570358100056463,"base_score":3.713572066704308,"endowment":3.713572066704308,"self_citation_contribution":0.5570358100056463,"citation_network_contribution":0.0,"self_endowment_contribution":0.5570358100056463,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":40,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":549228,"name":"Janeen L. Vanhooke","orcid":null,"position":1,"is_corresponding":false},{"id":1744852,"name":"Jean M. Prahl","orcid":null,"position":2,"is_corresponding":false},{"id":1744853,"name":"Hector F. DeLuca","orcid":null,"position":3,"is_corresponding":false},{"id":532599,"name":"Kevin D. Healy","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Parathyroid hormone decreases renal vitamin D receptor expression\n                    <i>in vivo</i>","abstract":"<jats:p>\n                    The vitamin D receptor (VDR) is a nuclear transcription factor responsible for mediating the biological activities of 1,25-dihydroxyvitamin D\n                    <jats:sub>3</jats:sub>\n                    [1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    ]. Renal and parathyroid gland VDR content is an important factor in calcium homeostasis, vitamin D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy. In these tissues, VDR expression is highly regulated by the calcium and vitamin D status. Although 1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastically reduced expression of the receptor. The generation of 25-hydroxyvitamin D\n                    <jats:sub>3</jats:sub>\n                    -1α-hydroxylase-null mice, which are incapable of endogenously producing 1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    , has allowed us to investigate the influence of parathyroid hormone (PTH) on VDR expression independent of PTH-mediated increases in 1,25(OH)\n                    <jats:sub>2</jats:sub>\n                    D\n                    <jats:sub>3</jats:sub>\n                    . Administration of human PTH (1-34) (110 μg/kg per day) for 48 h reduced renal VDR levels from 515 to 435 fmol/mg protein (15%,\n                    <jats:italic>P</jats:italic>\n                    &lt; 0.03) in wild-type mice. In the 25-hydroxyvitamin D\n                    <jats:sub>3</jats:sub>\n                    -1α-hydroxylase-null mice, PTH administration strongly reduced renal VDR levels, from 555 to 394 fmol/mg protein (29%,\n                    <jats:italic>P</jats:italic>\n                    &lt; 0.001). These results demonstrate that PTH is a potent down-regulator of VDR expression\n                    <jats:italic>in vivo</jats:italic>\n                    .\n                  </jats:p>","is_dataset_classified":null,"base_score":3.713572066704308,"endowment":3.713572066704308,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"15769857","pmcid":"PMC555704","openalex_id":"https://openalex.org/W1984501300","authors":[],"funders":[],"total_grants":0,"fwci":2.6959,"citation_percentile":0.88862614,"influential_citations":0,"citation_trend":[{"year":2012,"count":2},{"year":2014,"count":2},{"year":2015,"count":2},{"year":2016,"count":1},{"year":2017,"count":3},{"year":2019,"count":2},{"year":2020,"count":3},{"year":2021,"count":2},{"year":2022,"count":2},{"year":2023,"count":2},{"year":2024,"count":1}],"oa_status":"green","license":null,"oa_locations":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/555704","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/555704","host_type":"repository"},{"url":"https://pnas.org/doi/pdf/10.1073/pnas.0501312102","host_type":"publisher"},{"url":"https://doi.org/10.1073/pnas.0501312102","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/15769857","host_type":"repository"},{"url":"http://europepmc.org/pmc/articles/PMC555704","host_type":"repository"}],"fields_of_study":["Vitamin D Research Studies","Parathyroid Disorders and Treatments","Effects and risks of endocrine disrupting chemicals"],"mesh_terms":["Animals","Calcium","Kidney","Mice, Inbred C57BL","Parathyroid Hormone","Phosphorus","Spectrophotometry, Atomic","Down-Regulation","DNA Primers","Receptors, Calcitriol","Mice, Knockout","Reverse Transcriptase Polymerase Chain Reaction","Mice"],"keywords":["Calcitriol receptor","Internal medicine","Endocrinology","Parathyroid hormone","Secondary hyperparathyroidism","Vitamin D and neurology","Hyperparathyroidism","Calcium metabolism","Receptor","Renal osteodystrophy","Chemistry","vitamin D deficiency","Homeostasis","Calcitriol","Calcium","Biology","Medicine","Kidney disease"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-13T20:25:20.546623Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}