ArticleArthritis and rheumatism2012
Association of cartilage-specific deletion of peroxisome proliferator-activated receptor γ with abnormal endochondral ossification and impaired cartilage growth and development in a murine model.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 56 citations in OpenAlex.
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- Subchondral H-type blood vessel formation aggravates articular cartilage degeneration through LEP-LEPR axis.Frontiers in medicine · 2026Article
- PPARγ regulates osteoarthritis chondrocytes apoptosis through caspase-3 dependent mitochondrial pathway.Scientific reports · 2024Article
- Comparison of Gene Expression Patterns in Articular Cartilage and Xiphoid Cartilage.Biochemical genetics · 2022Article
- Adipokine Signaling Pathways in Osteoarthritis.Frontiers in bioengineering and biotechnology · 2022Review
- Effect Of XBP1 Deficiency In Cartilage On The Regulatory Network Of LncRNA/circRNA-miRNA-mRNA.International journal of biological sciences · 2022Article
- PFAS and Potential Adverse Effects on Bone and Adipose Tissue Through Interactions With PPARγ.Endocrinology · 2021Review
- Losartan protects against osteoarthritis by repressing the TGF-β1 signaling pathwayJournal of orthopaedic translation · 2021Article
- Transcriptional networks controlling stromal cell differentiation.Nature reviews. Molecular cell biology · 2021Review
- Genetic Variants and Protein Alterations of Selenium- and T-2 Toxin-Responsive Genes Are Associated With Chondrocytic Damage in Endemic Osteoarthropathy.Frontiers in genetics · 2021Article
- PPAR-δ agonist affects adipo-chondrogenic differentiation of human mesenchymal stem cells through the expression of PPAR-γ.Regenerative therapy · 2020Article
- MicroRNA-27b targets CBFB to inhibit differentiation of human bone marrow mesenchymal stem cells into hypertrophic chondrocytes.Stem cell research & therapy · 2020Article
- Article
- Upper Airway Obstruction Elicited Energy Imbalance Leads to Growth Retardation that Persists after the Obstruction Removal.Scientific reports · 2020Article
- Physiologic and pathologic effects of dietary free fatty acids on cells of the joint.Annals of the New York Academy of Sciences · 2019Review
- Endoglin haploinsufficiency is associated with differential regulation of extracellular matrix production during skin fibrosis and cartilage repair in mice.Journal of cell communication and signaling · 2018Article
- Article
- Abnormal Growth and Feeding Behavior in Upper Airway Obstruction in Rats.Frontiers in endocrinology · 2018Review
- Nuclear receptors regulate lipid metabolism and oxidative stress markers in chondrocytes.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Transcriptional control of chondrocyte specification and differentiation.Seminars in cell & developmental biology · 2017Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveLong bones develop through the strictly regulated process of endochondral ossification within the growth plate, resulting in the replacement of cartilage by bone. Defects in this process can result in skeletal abnormalities and a predisposition to degenerative joint diseases such as osteoarthritis (OA). Studies suggest that activation of the transcription factor peroxisome proliferator-activated receptor γ (PPARγ) is an important therapeutic target in OA. To devise PPARγ-related therapies in OA, it is critical to identify the role of this transcription factor in cartilage biology. Therefore, this study sought to determine the in vivo role of PPARγ in endochondral ossification and cartilage development, using cartilage-specific PPARγ-knockout (KO) mice.
methodsCartilage-specific PPARγ-KO mice were generated using the Cre/loxP system. Histomorphometric and immunohistochemical analyses were performed to assess the patterns of ossification, proliferation, differentiation, and hypertrophy of chondrocytes, skeletal organization, bone density, and calcium deposition in the KO mice.
resultsPPARγ-KO mice exhibited reductions in body length, body weight, length of the long bones, skeletal growth, cellularity, bone density, calcium deposition, and trabecular bone thickness, abnormal organization of the growth plate, loss of columnar organization, shorter hypertrophic zones, and delayed primary and secondary ossification. Immunohistochemical analyses for Sox9, 5-bromo-2'-deoxyuridine, p57, type X collagen, and platelet endothelial cell adhesion molecule 1 revealed reductions in the differentiation, proliferation, and hypertrophy of chondrocytes and in vascularization of the growth plate in mutant mice. Isolated chondrocytes and cartilage explants from mutant mice showed aberrant expression of Sox9 and extracellular matrix markers, including aggrecan, type II collagen, and matrix metalloproteinase 13. In addition, chondrocytes from mutant mice exhibited enhanced phosphorylation of p38 and decreased expression of Indian hedgehog.
conclusionThe presence of PPARγ is required for normal endochondral ossification and cartilage development in vivo.
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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.