ArticlePloS one2014
Hypertrophic chondrocytes in the rabbit growth plate can proliferate and differentiate into osteogenic cells when capillary invasion is interposed by a membrane filter.
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 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Depletion of b-series ganglioside prevents limb length discrepancy after growth plate injury.BMC musculoskeletal disorders · 2024Article
- Wnt/ß-catenin-mediated p53 suppression is indispensable for osteogenesis of mesenchymal progenitor cells.Cell death & disease · 2021Article
- Chondrogenesis Defines Future Skeletal Patterns Via Cell Transdifferentiation from Chondrocytes to Bone Cells.Current osteoporosis reports · 2020Review
- The Actions of IGF-1 in the Growth Plate and Its Role in Postnatal Bone Elongation.Current osteoporosis reports · 2020Review
- A Second Career for Chondrocytes-Transformation into Osteoblasts.Current osteoporosis reports · 2019Review
- Postnatal ex vivo rat model for longitudinal bone growth investigations.Animal models and experimental medicine · 2019Article
- Multifunctional molecule ERp57: From cancer to neurodegenerative diseases.Pharmacology & therapeutics · 2018Review
- The Chondro-Osseous Continuum: Is It Possible to Unlock the Potential Assigned Within?Frontiers in bioengineering and biotechnology · 2018Review
- Runx2 mediated Induction of Novel Targets ST2 and Runx3 Leads to Cooperative Regulation of Hypertrophic Differentiation in ATDC5 Chondrocytes.Scientific reports · 2017Article
- Dysregulated PDGFRα signaling alters coronal suture morphogenesis and leads to craniosynostosis through endochondral ossification.Development (Cambridge, England) · 2017Article
- Specific ablation of mouse Fam20C in cells expressing type I collagen leads to skeletal defects and hypophosphatemia.Scientific reports · 2017Article
- Roles of Chondrocytes in Endochondral Bone Formation and Fracture Repair.Journal of dental research · 2017Review
- Deficiency and Also Transgenic Overexpression of Timp-3 Both Lead to Compromised Bone Mass and Architecture In Vivo.PloS one · 2016Article
- Chondrocytes Directly Transform into Bone Cells in Mandibular Condyle Growth.Journal of dental research · 2015Article
- Dual pathways to endochondral osteoblasts: a novel chondrocyte-derived osteoprogenitor cell identified in hypertrophic cartilage.Biology open · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fate of hypertrophic chondrocytes during endochondral ossification remains controversial. It has long been thought that the calcified cartilage is invaded by blood vessels and that new bone is deposited on the surface of the eroded cartilage by newly arrived cells. The present study was designed to determine whether hypertrophic chondrocytes were destined to die or could survive to participate in new bone formation. In a rabbit experiment, a membrane filter with a pore size of 1 µm was inserted in the middle of the hypertrophic zone of the distal growth plate of ulna. In 33 of 37 animals, vascular invasion was successfully interposed by the membrane filter. During 8 days, the cartilage growth plate was enlarged, making the thickness 3-fold greater than that of the nonoperated control side. Histological examination demonstrated that the hypertrophic zone was exclusively elongated. At the terminal end of the growth plate, hypertrophic chondrocytes extruded from their territorial matrix into the open cavity on the surface of the membrane filter. The progenies of hypertrophic chondrocytes (PHCs) were PCNA positive and caspase-3 negative. In situ hybridization studies demonstrated that PHCs did not express cartilage matrix proteins anymore but expressed bone matrix proteins. Immunohistochemical studies also demonstrated that the new matrix produced by PHCs contained type I collagen, osteonectin, and osteocalcin. Based on these results, we concluded that hypertrophic chondrocytes switched into bone-forming cells after vascular invasion was interposed in the normal growth plate.
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