ArticleScientific reports2017
Transforming Growth Factor Beta is regulated by a Glucocorticoid-Dependent Mechanism in Denervation Mouse Bone.
Article in Scientific reports, 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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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Constitutive activation of TGF-β receptor type I promotes cortical and cancellous bone formation in adult mice.PloS one · 2026Article
- Apoptosis-related genes bridge inflammatory bowel disease and osteoporosis: A bioinformatic analysis.PloS one · 2026Article
- Bidirectional Interaction Between the Brain and Bone in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Analysis of the impact of different schemes of preparation to trabeculectomy on the healing markers on the Tenon fibroblasts cultures.Scientific reports · 2023Article
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone.Current osteoporosis reports · 2023Review
- Review
- Pathogenic mechanisms of glucocorticoid-induced osteoporosis.Cytokine & growth factor reviews · 2023Review
- Influence of exposure to microbial ligands, immunosuppressive drugs and chronic kidney disease on endogenous immunomodulatory gene expression in feline adipose-derived mesenchymal stem cells.Journal of feline medicine and surgery · 2022Article
- Article
- Mechanism of traumatic heterotopic ossification: In search of injury-induced osteogenic factors.Journal of cellular and molecular medicine · 2020Review
- Article
- TGF-β prevents the denervation-induced reduction of bone formation and promotes the bone regeneration through inhibiting ubiquitin-proteasome pathway.Bioscience reports · 2019Article
- Bone remodeling induced by mechanical forces is regulated by miRNAs.Bioscience reports · 2018Review
- The molecular etiology and treatment of glucocorticoid-induced osteoporosis.Tzu chi medical journalReview
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone growth and remodeling is inhibited by denervation in adults and children, resulting in alterations of linear growth and bone mass and increased risk for osteoporosis and pathologic fractures. Transforming growth factor beta (TGF-β) isoforms are a key group of growth factors that enhance bone formation. To explore the relation between denervation-induced reduction of bone formation and TGF-β gene expression, we measured mRNA levels of TGF-β in denervation mouse bone and found decreased mRNA levels of TGF-β1, TGF-β2 and TGF-β3. These changes were accompanied by diminishing weight loss, bone mineral density (BMD), trabecular thickness, trabecular separation and trabecular number of femur and lumbar, serum osteocalcin, total calcium, intact parathyroid hormone, and increased serum C telopeptide. Recombinant human TGF-β1 (rhTGF-β1) prevented denervation-induced reduction of BMD further supporting our hypothesis that denervation-induced reduction of bone formation is a result of inhibition of TGF-β gene expression. In addition, antiprogestins RU 38486 blunted the denervation-induced decrease in mRNA levels of TGF-β group, while dexamethasone (DEX) decreased TGF-β group mRNA levels in normal mice. Furthermore, the denervated-mice exhibited a threefold increase in plasma corticosterone. These results suggest that denervation-induced reduction of bone formation may be regulated by glucocorticoids via inhibition of TGF-β gene expression at least in part.
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