ArticleMolecular and cellular biology2011
Osteoclast progenitors reside in the peroxisome proliferator-activated receptor γ-expressing bone marrow cell population.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 46 citations in OpenAlex.
- Pioglitazone and Risk for Bone Fracture: Safety Data From a Randomized Clinical Trial.The Journal of clinical endocrinology and metabolism · 2017Trial
- Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025Review
- Towards an enhanced understanding of osteoanabolic effects of PTH-induced microRNAs on osteoblasts using a bioinformatic approach.Frontiers in endocrinology · 2024Article
- Pioglitazone and barriers to effective post-stroke comorbidity management in stroke survivors with diabetes.Neurosciences (Riyadh, Saudi Arabia) · 2024Article
- CSF1R as a Therapeutic Target in Bone Diseases: Obvious but Not so Simple.Current osteoporosis reports · 2022Review
- Monocyte-Macrophage Lineage Cell Fusion.International journal of molecular sciences · 2022Review
- Integrated computational and in vivo models reveal Key Insights into macrophage behavior during bone healing.PLoS computational biology · 2022Article
- Bone marrow adiposity during pathologic bone loss: molecular mechanisms underlying the cellular events.Journal of molecular medicine (Berlin, Germany) · 2022Review
- The Macrophage-Osteoclast Axis in Osteoimmunity and Osteo-Related Diseases.Frontiers in immunology · 2021Review
- A Panoply of Rheumatological Manifestations in Patients with GATA2 Deficiency.Scientific reports · 2020Review
- At the Crossroads of the Adipocyte and Osteoclast Differentiation Programs: Future Therapeutic Perspectives.International journal of molecular sciences · 2020Review
- Molecular determinants for the polarization of macrophage and osteoclast.Seminars in immunopathology · 2019Review
- Article
- Loss of the Hematopoietic Stem Cell Factor GATA2 in the Osteogenic Lineage Impairs Trabecularization and Mechanical Strength of Bone.Molecular and cellular biology · 2018Article
- The multi-faceted role of retinoid X receptor in bone remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Lipid Osteoclastokines Regulate Breast Cancer Bone Metastasis.Endocrinology · 2017Article
- PPAR-γ regulates pharmacological but not physiological or pathological osteoclast formation.Nature medicine · 2016Article
- Gata2 Is a Rheostat for Mesenchymal Stem Cell Fate in Male Mice.Endocrinology · 2016Article
- A Liver-Bone Endocrine Relay by IGFBP1 Promotes Osteoclastogenesis and Mediates FGF21-Induced Bone Resorption.Cell metabolism · 2015Article
- Cthrc1 controls adipose tissue formation, body composition, and physical activity.Obesity (Silver Spring, Md.) · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Osteoclasts are bone-resorbing cells essential for skeletal development, homeostasis, and regeneration. They derive from hematopoietic progenitors in the monocyte/macrophage lineage and differentiate in response to RANKL. However, the precise nature of osteoclast progenitors is a longstanding and important question. Using inducible peroxisome proliferator-activated receptor γ (PPARγ)-tTA TRE-GFP (green fluorescent protein) reporter mice, we show that osteoclast progenitors reside specifically in the PPARγ-expressing hematopoietic bone marrow population and identify the quiescent PPARγ(+) cells as osteoclast progenitors. Importantly, two PPARγ-tTA TRE-Cre-controlled genetic models provide compelling functional evidence. First, Notch activation in PPARγ(+) cells causes high bone mass due to impaired osteoclast precursor proliferation. Second, selective ablation of PPARγ(+) cells by diphtheria toxin also causes high bone mass due to decreased osteoclast numbers. Furthermore, PPARγ(+) cells respond to both pathological and pharmacological resorption-enhancing stimuli. Mechanistically, PPARγ promotes osteoclast progenitors by activating GATA2 transcription. These findings not only identify the long-sought-after osteoclast progenitors but also establish unprecedented tools for their visualization, isolation, characterization, and genetic manipulation.
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What OpenQuestion holds
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.