The Increase in FGF23 Induced by Calcium Is Partially Dependent on Vitamin D Signaling
BACKGROUND: Increased FGF23 levels are an early pathological feature in chronic kidney disease (CKD), causing increased cardiovascular risk. The regulation of FGF23 expression is complex and not completely understood. Thus, Ca2+ has been shown to induce an increase in FGF23 expression, but whether that increase is mediated by simultaneous changes in parathyroid hormone (PTH) and/or vitamin D is not fully known.
METHODS: Osteoblast-like cells (OLCs) from vitamin D receptor (VDR)+/+ and VDR-/- mice were incubated with Ca2+ for 18 h. Experimental hypercalcemia was induced by calcium gluconate injection in thyro-parathyroidectomized (T-PTX) VDR +/+ and VDR-/- mice with constant PTH infusion.
RESULTS: Inorganic Ca2+ induced an increase in FGF23 gene and protein expression in osteoblast-like cells (OLCs), but the increase was blunted in cells lacking VDR. In T-PTX VDR +/+ and VDR-/- mice with constant PTH levels, hypercalcemia induced an increase in FGF23 levels, but to a lower extent in animals lacking VDR. Similar results were observed in FGF23 expression in bone. Renal and bone 1α-hydroxylase expression was also modulated.
CONCLUSIONS: Our study demonstrates that Ca2+ can increase FGF23 levels independently of vitamin D and PTH, but part of the physiological increase in FGF23 induced by Ca2+ is mediated by vitamin D signaling.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2022 |
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Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - volume:14 |
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Enthalten in: |
Nutrients - 14(2022), 13 vom: 22. Juni |
Sprache: |
Englisch |
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Beteiligte Personen: |
Rayego-Mateos, Sandra [VerfasserIn] |
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Links: |
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Themen: |
1406-16-2 |
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Anmerkungen: |
Date Completed 12.07.2022 Date Revised 20.07.2022 published: Electronic Citation Status MEDLINE |
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doi: |
10.3390/nu14132576 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM343282461 |
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520 | |a BACKGROUND: Increased FGF23 levels are an early pathological feature in chronic kidney disease (CKD), causing increased cardiovascular risk. The regulation of FGF23 expression is complex and not completely understood. Thus, Ca2+ has been shown to induce an increase in FGF23 expression, but whether that increase is mediated by simultaneous changes in parathyroid hormone (PTH) and/or vitamin D is not fully known | ||
520 | |a METHODS: Osteoblast-like cells (OLCs) from vitamin D receptor (VDR)+/+ and VDR-/- mice were incubated with Ca2+ for 18 h. Experimental hypercalcemia was induced by calcium gluconate injection in thyro-parathyroidectomized (T-PTX) VDR +/+ and VDR-/- mice with constant PTH infusion | ||
520 | |a RESULTS: Inorganic Ca2+ induced an increase in FGF23 gene and protein expression in osteoblast-like cells (OLCs), but the increase was blunted in cells lacking VDR. In T-PTX VDR +/+ and VDR-/- mice with constant PTH levels, hypercalcemia induced an increase in FGF23 levels, but to a lower extent in animals lacking VDR. Similar results were observed in FGF23 expression in bone. Renal and bone 1α-hydroxylase expression was also modulated | ||
520 | |a CONCLUSIONS: Our study demonstrates that Ca2+ can increase FGF23 levels independently of vitamin D and PTH, but part of the physiological increase in FGF23 induced by Ca2+ is mediated by vitamin D signaling | ||
650 | 4 | |a Journal Article | |
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700 | 1 | |a Valdivielso, Jose Manuel |e verfasserin |4 aut | |
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