<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bacchetta J</submitter><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NIAMS NIH HHS</funding><pagination>46-55</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3511915</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>28(1)</volume><pubmed_abstract>Vitamin D is a potent stimulator of monocyte innate immunity, and this effect is mediated via intracrine conversion of 25-hydroxyvitamin D (25OHD) to 1,25-dihydroxyvitamin D (1,25(OH)(2) D). In the kidney, synthesis of 1,25(OH)(2) D is suppressed by fibroblast growth factor 23 (FGF23), via transcriptional suppression of the vitamin D-activating enzyme 1α-hydroxylase (CYP27B1). We hypothesized that FGF23 also suppresses CYP27B1 in monocytes, with concomitant effects on intracrine responses to 1,25(OH)(2) D. Healthy donor peripheral blood mononuclear cell monocytes (PBMCm) and peritoneal dialysate monocyte (PDm) effluent from kidney disease patients were assessed at baseline to confirm the presence of mRNA for FGF23 receptors (FGFRs), with Klotho and FGFR1 being more strongly expressed than </pubmed_abstract><journal>Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research</journal><pubmed_title>Fibroblast growth factor 23 inhibits extrarenal synthesis of 1,25-dihydroxyvitamin D in human monocytes.</pubmed_title><pmcid>PMC3511915</pmcid><funding_grant_id>P50 AR063020</funding_grant_id><funding_grant_id>P30 AI028697</funding_grant_id><funding_grant_id>K23 DK080984</funding_grant_id><funding_grant_id>UL1 TR000124</funding_grant_id><funding_grant_id>R01 DK067563</funding_grant_id><funding_grant_id>DK 67563</funding_grant_id><funding_grant_id>UL1 RR033176</funding_grant_id><funding_grant_id>R21 DK091672</funding_grant_id><funding_grant_id>DK 80984</funding_grant_id><funding_grant_id>DK 35423</funding_grant_id><funding_grant_id>R01 DK035423</funding_grant_id><funding_grant_id>DK0911672</funding_grant_id><pubmed_authors>Bacchetta J</pubmed_authors><pubmed_authors>Lisse TS</pubmed_authors><pubmed_authors>Gales B</pubmed_authors><pubmed_authors>Hewison M</pubmed_authors><pubmed_authors>Wesseling-Perry K</pubmed_authors><pubmed_authors>Salusky IB</pubmed_authors><pubmed_authors>Adams JS</pubmed_authors><pubmed_authors>Chun RF</pubmed_authors><pubmed_authors>Sea JL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Fibroblast growth factor 23 inhibits extrarenal synthesis of 1,25-dihydroxyvitamin D in human monocytes.</name><description>Vitamin D is a potent stimulator of monocyte innate immunity, and this effect is mediated via intracrine conversion of 25-hydroxyvitamin D (25OHD) to 1,25-dihydroxyvitamin D (1,25(OH)(2) D). In the kidney, synthesis of 1,25(OH)(2) D is suppressed by fibroblast growth factor 23 (FGF23), via transcriptional suppression of the vitamin D-activating enzyme 1α-hydroxylase (CYP27B1). We hypothesized that FGF23 also suppresses CYP27B1 in monocytes, with concomitant effects on intracrine responses to 1,25(OH)(2) D. Healthy donor peripheral blood mononuclear cell monocytes (PBMCm) and peritoneal dialysate monocyte (PDm) effluent from kidney disease patients were assessed at baseline to confirm the presence of mRNA for FGF23 receptors (FGFRs), with Klotho and FGFR1 being more strongly expressed than </description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Jan</publication><modification>2025-04-03T23:34:06.932Z</modification><creation>2019-03-27T01:01:18Z</creation></dates><accession>S-EPMC3511915</accession><cross_references><pubmed>22886720</pubmed><doi>10.1002/jbmr.1740</doi></cross_references></HashMap>