ArticleEndocrinology2010
Transforming growth factor-{beta} coordinately induces suppressor of cytokine signaling 3 and leukemia inhibitory factor to suppress osteoclast apoptosis.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Direct and indirect effects of transforming growth factor-beta on osteoclast-mediated bone remodeling using a new in vitro bone matrix model.JBMR plus · 2025Article
- The protective effect of leukemia inhibitory factor on apoptosis of BMSCs induced by hypoxia and serum-deprivation.American journal of translational research · 2023Article
- Novel insights into the coupling of osteoclasts and resorption to bone formation.Seminars in cell & developmental biology · 2022Review
- New insights intoFrontiers in cellular and infection microbiology · 2022Review
- New Insights Into Osteoclast Biology.JBMR plus · 2021Review
- Non-Coding RNAs in Multiple Myeloma Bone Disease Pathophysiology.Non-coding RNA · 2020Review
- Sclerostin expression in trabecular bone is downregulated by osteoclasts.Scientific reports · 2020Article
- Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases.Frontiers in physiology · 2020Review
- Positive and negative regulators of osteoclast apoptosis.Bone reports · 2019Review
- Glucagon-like peptide 2 decreases osteoclasts by stimulating apoptosis dependent on nitric oxide synthase.Cell proliferation · 2018Article
- Therapeutic and Preventive Effects of Osteoclastogenesis Inhibitory Factor on Osteolysis, Proliferation of Mammary Tumor Cell and Induction of Cancer Stem Cells in the Bone Microenvironment.International journal of molecular sciences · 2018Article
- Stimulation of osteoclast migration and bone resorption by C-C chemokine ligands 19 and 21.Experimental & molecular medicine · 2017Article
- Inhibition of Transforming Growth Factor-β Activation Diminishes Tumor Progression and Osteolytic Bone Disease in Mouse Models of Multiple Myeloma.The American journal of pathology · 2016Article
- Rhizoma Dioscoreae extract protects against alveolar bone loss in ovariectomized rats via microRNAs regulation.Nutrients · 2015Article
- PhenomeExpress: a refined network analysis of expression datasets by inclusion of known disease phenotypes.Scientific reports · 2015Article
- Stüve-Wiedemann syndrome: LIFR and associated cytokines in clinical course and etiology.Orphanet journal of rare diseases · 2014Review
- Role of suppressors of cytokine signaling 3 in bone inflammatory responses.Frontiers in immunology · 2014Review
- STAT3 modulates cigarette smoke-induced inflammation and protease expression.Frontiers in physiology · 2013Article
- Thrombospondin-1 inhibits osteogenic differentiation of human mesenchymal stem cells through latent TGF-β activation.Biochemical and biophysical research communications · 2012Article
- Extensive mannose phosphorylation on leukemia inhibitory factor (LIF) controls its extracellular levels by multiple mechanisms.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Local release of TGF-beta during times of high bone turnover leads to elevated levels within the bone microenvironment, and we have shown that TGF-beta suppresses osteoclast apoptosis. Therefore, understanding the influences of TGF-beta on bone resorbing osteoclasts is critical to the design of therapies to reduce excess bone loss. Here we investigated the mechanisms by which TGF-beta sustains suppression of osteoclast apoptosis. We found TGF-beta rapidly increased leukemia inhibitory factor (LIF) expression and secretion by phosphorylated mothers against decapentaplegic-dependent and -independent signaling pathways. TGF-beta also induced suppressor of cytokine signaling 3 (SOCS3) expression, which was required for TGF-beta or LIF to promote osteoclast survival by. Blocking LIF or SOCS3 blocked TGF-beta promotion of osteoclast survival, confirming that LIF and SOCS3 expression are necessary for TGF-beta-mediated suppression of osteoclast apoptosis. Investigation of the mechanisms by which LIF promotes osteoclast survival revealed that LIF-induced expression of Bcl-X(L) and repressed Bcl-2 interacting domain expression by activating MAPK kinase, AKT, and nuclear factor-kappaB pathways. Suppression of Janus kinase/signal transducer and activator of transcription signaling further increased Bcl-X(L) expression and enhanced osteoclast survival, supporting that this pathway is not involved in prosurvival effects of TGF-beta and LIF. These data show that TGF-beta coordinately induces LIF and SOCS3 to promote prosurvival signaling. This alters the ratio of prosurvival Bcl2 family member Bcl-X(L) to proapoptotic family member Bcl-2 interacting domain, leading to prolonged osteoclast survival.
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Registered trials
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