ArticleStem cells (Dayton, Ohio)2013
Osteoblast-targeted suppression of PPARγ increases osteogenesis through activation of mTOR signaling.
Article in Stem cells (Dayton, Ohio), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 85 citations in OpenAlex.
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- Developmentally Inspired, Mechanical-Metabolic Dual Gradient Osteochondral Constructs Bridging Regeneration and Therapeutic Screening.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FTO-mediated m6A modification regulates the osteogenic differentiation of ADSCs by targeting FOXO1.Stem cell research & therapy · 2025Article
- The Crosstalk Between B Cells and the Skeletal System During Development, Aging, and in Pathological Conditions.Current osteoporosis reports · 2025Review
- Fat Mass and Obesity-Associated Protein-Mediated Adipogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Promotes Chemotherapy Resistance in Acute Myeloid LeukemiaBalkan medical journal · 2025Article
- Extracellular derivatives for bone metabolism.Journal of advanced research · 2024Review
- Targeting the mTOR-Autophagy Axis: Unveiling Therapeutic Potentials in Osteoporosis.Biomolecules · 2024Review
- Effects of Systemic Peroxisome Proliferator-Activated Receptor Gamma Inhibition on Bone and Immune Cells in Aged Female Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Selective Inhibition of mTORC1 Signaling Supports the Development and Maintenance of Pluripotency.Stem cells (Dayton, Ohio) · 2024Article
- CCL3 in the bone marrow microenvironment causes bone loss and bone marrow adiposity in aged mice.JCI insight · 2023Article
- Article
- Peroxisome Proliferator-Activated ReceptorPPAR research · 2023Article
- PPARγ/mTOR Regulates the Synthesis and Release of Prostaglandins in Ovine Trophoblast Cells in Early Pregnancy.Veterinary sciences · 2022Article
- High-energy extracorporeal shockwave therapy in humeral delayed and non-unions.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Berberine ameliorates the LPS-induced imbalance of osteogenic and adipogenic differentiation in rat bone marrow-derived mesenchymal stem cells.Molecular medicine reports · 2021Article
- Lack of Adiponectin Drives Hyperosteoclastogenesis in Lipoatrophic Mice.Frontiers in cell and developmental biology · 2021Article
- Article
- Increased marrow adipogenesis does not contribute to age-dependent appendicular bone loss in female mice.Aging cell · 2020Article
- LncRNA LOXL1-AS1 controls osteogenic and adipocytic differentiation of bone marrow mesenchymal stem cells in postmenopausal osteoporosis through regulating the miR-196a-5p/Hmga2 axis.Journal of bone and mineral metabolism · 2020Article
- Deletion of PPARγ in Mesenchymal Lineage Cells Protects Against Aging-Induced Cortical Bone Loss in Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Nuclear receptor peroxisome proliferator-activated receptor-γ (PPARγ) is an essential transcription factor for adipocyte differentiation. In mesenchymal stem cells, PPARγ has been assumed to play a negative role in osteoblastic differentiation, by working in an adipogenesis dependent manner, due to the reciprocal relationship between osteoblast and adipocyte differentiation. However, the direct role of PPARγ in osteoblast function is not fully understood, due in part to inadequate model systems. Here, we describe an adenoviral-mediated PPARγ knockout system in which suppression of PPARγ in mesenchymal stem cells enhanced osteoblast differentiation and inhibited adipogenesis in vitro. Consistent with this in vitro observation, lipoatrophic A-ZIP/F1 mice, which do not form adipocytes, displayed a phenotype in which both cortical and trabecular bone was significantly increased compared with wild-type mice. We next developed an inducible osteoblast-targeted PPARγ knockout (Osx Cre/flox- PPARγ) mouse to determine the direct role of PPARγ in bone formation. Data from both in vitro cultures of mesenchymal stem cells and in vivo µCT analysis of bones suggest that suppression of PPARγ activity in osteoblasts significantly increased osteoblast differentiation and trabecular number. Endogenous PPARγ in mesenchymal stem cells and osteoblasts strongly inhibited Akt/mammalian target of rapamycin (mTOR)/p70S6k activity and led to decreased osteoblastic differentiation. Therefore, we conclude that PPARγ modulates osteoblast differentiation and bone formation through both direct and indirect mechanisms. The direct mode, as shown here, involves PPARγ regulation of the mTOR pathway, while the indirect pathway is dependent on the regulation of adipogenesis.
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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.