ArticleJournal of cellular physiology2017
Glucocorticoids Hijack Runx2 to Stimulate Wif1 for Suppression of Osteoblast Growth and Differentiation.
Article in Journal of cellular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Dysregulation of the MACF1-Rab14/KIF16B-FGFR Vesicular Trafficking Axis Skews MSC Lineage Commitment in Glucocorticoid-Induced Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of wnt signaling in diabetes-induced osteoporosis.Diabetology & metabolic syndrome · 2023Review
- Activation of dopamine receptor D1 promotes osteogenic differentiation and reduces glucocorticoid-induced bone loss by upregulating the ERK1/2 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2022Article
- Trabecular bone score and sclerostin concentrations in patients with primary adrenal insufficiency.Frontiers in endocrinology · 2022Article
- Activation of cannabinoid receptor 2 alleviates glucocorticoid-induced osteonecrosis of femoral head with osteogenesis and maintenance of blood supply.Cell death & disease · 2021Article
- Nuclear receptors in osteoclasts.Current opinion in pharmacology · 2020Review
- Improved Glucocorticoid Receptor Ligands: Fantastic Beasts, but How to Find Them?Frontiers in endocrinology · 2020Review
- A Jack of All Trades: Impact of Glucocorticoids on Cellular Cross-Talk in Osteoimmunology.Frontiers in immunology · 2019Review
- Estrogens and selective estrogen receptor modulators differentially antagonize Runx2 in ST2 mesenchymal progenitor cells.The Journal of steroid biochemistry and molecular biology · 2018Article
- Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo.Scientific reports · 2018Article
- Valproic acid prevents glucocorticoid‑induced osteonecrosis of the femoral head of rats.International journal of molecular medicine · 2018Article
- Estrogens and androgens inhibit association of RANKL with the pre-osteoblast membrane through post-translational mechanisms.Journal of cellular physiology · 2017Article
- Treatment with hydrogen sulfide attenuates sublesional skeletal deterioration following motor complete spinal cord injury in rats.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2017Article
- Arginine methylation of R81 in Smad6 confines BMP-induced Smad1 signaling.The Journal of biological chemistryArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Inhibition of Runx2 is one of many mechanisms that suppress bone formation in glucocorticoid (GC)-induced osteoporosis (GIO). We profiled mRNA expression in ST2/Rx2(dox) cells after treatment with doxycycline (dox; to induce Runx2) and/or the synthetic GC dexamethasone (dex). As expected, dex typically antagonized Runx2-driven transcription. Select genes, however, were synergistic stimulated and this was confirmed by RT-qPCR. Among the genes synergistically stimulated by GCs and Runx2 was Wnt inhibitory Factor 1 (Wif1), and Wif1 protein was readily detectable in medium conditioned by cultures co-treated with dox and dex, but neither alone. Cooperation between Runx2 and GCs in stimulating Wif1 was also observed in primary preosteoblast cultures. GCs strongly inhibited dox-driven alkaline phosphatase (ALP) activity in control ST2/Rx2(dox) cells, but not in cells in which Wif1 was silenced. Unlike its anti-mitogenic activity in committed osteoblasts, induction of Runx2 transiently increased the percentage of cells in S-phase and accelerated proliferation in the ST2 mesenchymal pluripotent cell culture model. Furthermore, like the inhibition of Runx2-driven ALP activity, dex antagonized the transient mitogenic effect of Runx2 in ST2/Rx2(dox) cultures, and this inhibition eased upon Wif1 silencing. Plausibly, homeostatic feedback loops that rely on Runx2 activation to compensate for bone loss in GIO are thwarted, exacerbating disease progression through stimulation of Wif1. J. Cell. Physiol. 232: 145-153, 2017. © 2016 Wiley Periodicals, Inc.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.