Adult cartilage-specific peroxisome proliferator-activated receptor gamma knockout mice exhibit the spontaneous osteoarthritis phenotype
Open accessAbstract
Osteoarthritis (OA) is an age-related progressive degenerative joint disease. Peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor, is suggested as an attractive therapeutic target to counteract degradative mechanisms associated with OA. Studies suggest that activation of PPARγ by its agonists can reduce the synthesis of OA catabolic and inflammatory factors and the development of cartilage lesions in OA animal models. Because these agonists impart several PPARγ-independent effects, the specific in vivo function of PPARγ in cartilage homeostasis and OA remains largely unknown. Herein, we describe the in vivo role of PPARγ in OA using cartilage-specific PPARγ knockout (KO) mice generated using the Cre-lox system. Adult PPARγ KO mice exhibited a spontaneous OA phenotype associated with enhanced cartilage degradation, hypocellularity, synovial and cartilage fibrosis, synovial inflammation, mononuclear cell influx in the synovium, and increased expression of catabolic factors, including matrix metalloproteinase-13, accompanied by an increase in staining for matrix metalloproteinase-generated aggrecan and type II collagen neoepitopes (VDIPEN and C1-2C). We demonstrate that PPARγ-deficient articular cartilage exhibits elevated expression of the additional catabolic factors hypoxia-inducible factor-2α, syndecan-4, and a disintegrin and metalloproteinase with thrombospondin motifs 5 and of the inflammatory factors cyclooxygenase-2 and inducible nitric oxide synthase. In conclusion, PPARγ is a critical regulator of cartilage health, the lack of which leads to an accelerated spontaneous OA phenotype.
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PPARγ has a protective role in articular cartilage.
“it has been demonstrated that PPARγ has a protective role in articular cartilage.”
From Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy (2019) · cites this paper as [56]
Cartilage-specific PPARγ deficient mice showed increased apoptosis, increased production of inflammatory and catabolic factors, decreased expression of anabolic factors, and accelerated OA.
“Cartilage-specific PPARγ deficient mice showed increased apoptosis as well as production of inflammatory and catabolic factors, and a decreased expression of anabolic factors, overall resulting in accelerated OA [56,57].”
From Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy (2019) · cites this paper as [56]
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- Authors
- Vasheghani, F., Monemdjou, R., Fahmi, H., Zhang, Y., Perez, G., Blati, M., St-Arnaud, R., Pelletier, J.-P., Beier, F., Martel-Pelletier, J., & Kapoor, M.
- Affiliations
- Université de Montréal (CA)
- Western University (CA)
- Corresponding author
- Kapoor, Mohit
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2013-04
- Volume
- 182
- Issue
- 4
- Pages
- 1099-1106
- ISSN
- 0002-9440 (ISSN-L)
- OpenAlex
- W2103103370
- Cited by
- 80
- References
- 39
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 2 · 2023: 8 · 2022: 7 · 2021: 2 · 2020: 8 · 2019: 8 · 2018: 7 · 2017: 5 · 2016: 8 · 2015: 8 · 2014: 8 · 2013: 1
- FWCI
- 6.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research (MOP219423)
- Fonds de Recherche du Québec - Santé
- Canada Foundation for Innovation
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- osteoarthritis, PPARγ, articular cartilage homeostasis, cartilage degeneration, synovitis, matrix metalloproteinase-13, aggrecan degradation, HIF-2α, syndecan-4, ADAMTS5, cyclooxygenase-2, inducible nitric oxide synthase, cartilage fibrosis, synovial fibrosis
- MeSH terms
- Aging, Animals, Cartilage, Fibrosis, Inflammation, Organ Specificity, Osteoarthritis, Phenotype, Synovial Membrane, Biomarkers, Gene Deletion, Mice, Knockout, Inflammation Mediators, PPAR gamma, Mice
About these checks
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