ArticleScientific reports2023
Oncostatin M is a regulator of fibroblast growth factor 23 (FGF23) in UMR106 osteoblast-like cells.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 2 citations in OpenAlex.
- Three-Phase Serum Concentration Kinetics of FGF23 in a Clinical Model of Acute Myocardial Infarction.Cells · 2026Article
- Celastrol Attenuates FGF23 Expression in Osteoblasts by Inhibiting STAT3 Activation.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Article
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3 authors at 1 institution in 1 country.
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Abstract
Renal phosphate and vitamin D metabolism is under the control of fibroblast growth factor 23 (FGF23), an endocrine and paracrine factor predominantly produced in bone. FGF23 formation is stimulated by active vitamin D, or parathyroid hormone (PTH), which are further regulators of phosphate homeostasis. In renal, inflammatory, and other diseases, plasma FGF23 reflects disease stage and correlates with outcome. Oncostatin M is part of the interleukin-6 (IL-6) family and regulates remodeling and PTH effects in bone as well as cardiac FGF23 production in heart failure via glycoprotein gp130. Here, we studied whether oncostatin M is a regulator of FGF23 in bone cells. Experiments were performed in UMR106 osteoblast-like cells, Fgf23 mRNA was determined by qRT-PCR, FGF23 protein by Western Blotting and ELISA, and oncostatin M receptor and leukemia inhibitory factor (LIF) receptor gene knockout accomplished by siRNA. As a result, oncostatin M dose-dependently up-regulated Fgf23 expression and protein secretion. The oncostatin M effect on FGF23 was mediated by oncostatin M receptor and gp130 and involved, at least in part, STAT3 and MEK1/2. Taken together, oncostatin M is a regulator of FGF23 through oncostatin M receptor, gp130, as well as STAT3 and MEK1/2 in UMR106 osteoblasts.
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