Oncostatin M is a regulator of fibroblast growth factor 23 (FGF23) in UMR106 osteoblast-like cells [18.08.23]
Fibroblast growth factor 23 (FGF23) is a protein that, together with its essential cofactor Klotho, plays an important role in phosphate metabolism. While sinking levels of Klotho and FGF23 increase signs of aging, an increase of FGF23 plasma concentration can be indicative for renal insufficiencies, cardiovascular diseases or oncogenic bone diseases. The control mechanisms of FGF23 production are therefore of great interest for the diagnosis and treatment of FGF23-related diseases. A current study of Michael Föller's research group investigates the regulatory role of oncostatin M as a member of the IL-6 cytokine family for the production of FGF23 in osteoblast-like cells.
Source: Rausch, S., Föller, M. (2022) The regulation of FGF23 under physiological and pathophysiological conditions
Original Study
Münz S., Feger M., Föller M. (2023) Oncostatin M is a regulator of fibroblast growth factor 23 (FGF23) in UMR106 osteoblast-like cells. Scientific Reports, 13 (1), art. no. 8420, DOI: 10.1038/s41598-023-34858-6
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. © 2023, The Author(s).
Diese Studie wurde durch die Deutsche Forschungsgemeinschaft, DFG, Fo 695/2-2 gefördert. All Open Access wird im Rahmen des Projektes DEAL ermöglicht.
Contact to the author
 | Professor Dr. Michael FöllerPhone: +49 711 459 24566 physiologie(at)uni-hohenheim.de |
