ArticlePloS one2014
Abnormal chondrocyte apoptosis in the cartilage growth plate is influenced by genetic background and deletion of CHOP in a targeted mouse model of pseudoachondroplasia.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.Bone research · 2025Article
- Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications.Cell stress & chaperones · 2024Review
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- Clinical, Biochemical, Radiological, Genetic and Therapeutic Analysis of Patients with COMP Gene Variants.Calcified tissue international · 2022Article
- Genetic Disorders of the Extracellular Matrix.Anatomical record (Hoboken, N.J. : 2007) · 2020Review
- Proteome analysis of human mesenchymal stem cells undergoing chondrogenesis when exposed to the products of various magnesium-based materials degradation.Bioactive materials · 2019Article
- A novel mutation in exon 11 of COMP gene in a Chinese family with pseudoachondroplasia.Genes & diseases · 2019Article
- Mesencephalic astrocyte-derived neurotropic factor is an important factor in chondrocyte ER homeostasis.Cell stress & chaperones · 2019Article
- Article
- Article
- Different Forms of ER Stress in Chondrocytes Result in Short Stature Disorders and Degenerative Cartilage Diseases: New Insights by Cartilage-Specific ERp57 Knockout Mice.Oxidative medicine and cellular longevity · 2018Review
- Antisense Reduction of Mutant COMP Reduces Growth Plate Chondrocyte Pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Emerging targets in osteoarthritis therapy.Current opinion in pharmacology · 2015Review
- The utility of mouse models to provide information regarding the pathomolecular mechanisms in human genetic skeletal diseases: The emerging role of endoplasmic reticulum stress (Review).International journal of molecular medicine · 2015Review
- The Chondroprotective Role of TMF in PGE2-Induced Apoptosis Associating with Endoplasmic Reticulum Stress.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Article
- Pseudoachondroplasia/COMP - translating from the bench to the bedside.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Pseudoachondroplasia (PSACH) is an autosomal dominant skeletal dysplasia caused by mutations in cartilage oligomeric matrix protein (COMP) and characterised by short limbed dwarfism and early onset osteoarthritis. Mouse models of PSACH show variable retention of mutant COMP in the ER of chondrocytes, however, in each case a different stress pathway is activated and the underlying disease mechanisms remain largely unknown. T585M COMP mutant mice are a model of moderate PSACH and demonstrate a mild ER stress response. Although mutant COMP is not retained in significant quantities within the ER of chondrocytes, both BiP and the pro-apoptotic ER stress-related transcription factor CHOP are mildly elevated, whilst bcl-2 levels are decreased, resulting in increased and spatially dysregulated chondrocyte apoptosis. To determine whether the abnormal chondrocyte apoptosis observed in the growth plate of mutant mice is CHOP-mediated, we bred T585M COMP mutant mice with CHOP-null mice to homozygosity, and analysed the resulting phenotype. Although abnormal apoptosis was alleviated in the resting zone following CHOP deletion, the mutant growth plates were generally more disorganised. Furthermore, the bone lengths of COMP mutant CHOP null mice were significantly shorter at 9 weeks of age when compared to the COMP mutant mice, including a significant difference in the skull length. Overall, these data demonstrate that CHOP-mediated apoptosis is an early event in the pathobiology of PSACH and suggest that the lack of CHOP, in conjunction with a COMP mutation, may lead to aggravation of the skeletal phenotype via a potentially synergistic effect on endochondral ossification.
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