ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2014
Deficiency of Sef is associated with increased postnatal cortical bone mass by regulating Runx2 activity.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Endothelial IL17RD promotes Western diet-induced aortic myeloid cell infiltration.Biochemical and biophysical research communications · 2024Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Interleukin-17 receptor D (Sef) is a multi-functional regulator of cell signaling.Cell communication and signaling : CCS · 2021Review
- Loss of interleukin-17 receptor D promotes chronic inflammation-associated tumorigenesis.Oncogene · 2021Article
- Interleukin-17 Receptor D in Physiology, Inflammation and Cancer.Frontiers in oncology · 2021Review
- A G protein-coupled, IP3/protein kinase C pathway controlling the synthesis of phosphaturic hormone FGF23.JCI insight · 2019Article
- Fenofibrate Inhibits Cytochrome P450 Epoxygenase 2C Activity to Suppress Pathological Ocular Angiogenesis.EBioMedicine · 2016Article
- Sulfated hydrogel matrices direct mitogenicity and maintenance of chondrocyte phenotype through activation of FGF signaling.Advanced functional materials · 2016Article
- The G protein α subunit variant XLαs promotes inositol 1,4,5-trisphosphate signaling and mediates the renal actions of parathyroid hormone in vivo.Science signaling · 2015Article
- Fibroblast growth factor signaling in the vasculature.Current atherosclerosis reports · 2015Review
- Optimization of an Image-Guided Laser-Induced Choroidal Neovascularization Model in Mice.PloS one · 2015Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Sef (similar expression to fgf genes) is a feedback inhibitor of fibroblast growth factor (FGF) signaling and functions in part by binding to FGF receptors and inhibiting their activation. Genetic studies in mice and humans indicate an important role for fibroblast growth factor signaling in bone growth and homeostasis. We, therefore, investigated whether Sef had a function role in skeletal acquisition and remodeling. Sef expression is increased during osteoblast differentiation in vitro, and LacZ staining of Sef+/- mice showed high expression of Sef in the periosteum and chondro-osseous junction of neonatal and adult mice. Mice with a global deletion of Sef showed increased cortical bone thickness, bone volume, and increased periosteal perimeter by micro-computed tomography (micro-CT). Histomorphometric analysis of cortical bone revealed a significant increase in osteoblast number. Interestingly, Sef-/- mice showed very little difference in trabecular bone by micro-CT and histomorphometry compared with wild-type mice. Bone marrow cells from Sef-/- mice grown in osteogenic medium showed increased proliferation and increased osteoblast differentiation compared with wild-type bone marrow cells. Bone marrow cells from Sef-/- mice showed enhanced FGF2-induced activation of the ERK pathway, whereas bone marrow cells from Sef transgenic mice showed decreased FGF2-induced signaling. FGF2-induced acetylation and stability of Runx2 was enhanced in Sef-/- bone marrow cells, whereas overexpression of Sef inhibited Runx2-responsive luciferase reporter activity. Bone marrow from Sef-/- mice showed enhanced hematopoietic lineage-dependent and osteoblast-dependent osteoclastogenesis and increased bone resorptive activity relative to wild-type controls in in vitro assays, whereas overexpression of Sef inhibited osteoclast differentiation. Taken together, these studies indicate that Sef has specific roles in osteoblast and osteoclast lineages and that its absence results in increased osteoblast and osteoclast activity with a net increase in cortical bone mass.
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