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Cell Death in Chondrocytes, Osteoblasts, and Osteocytes

Department of Cell Biology, Unit of Basic Medical Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8588, Japan
Academic Editor: Anthony Lemarié
Int. J. Mol. Sci. 2016, 17(12), 2045; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17122045
Received: 14 July 2016 / Revised: 13 November 2016 / Accepted: 23 November 2016 / Published: 6 December 2016
(This article belongs to the Collection Programmed Cell Death and Apoptosis)
Cell death in skeletal component cells, including chondrocytes, osteoblasts, and osteocytes, plays roles in skeletal development, maintenance, and repair as well as in the pathogenesis of osteoarthritis and osteoporosis. Chondrocyte proliferation, differentiation, and apoptosis are important steps for endochondral ossification. Although the inactivation of P53 and RB is involved in the pathogenesis of osteosarcomas, the deletion of p53 and inactivation of Rb are insufficient to enhance chondrocyte proliferation, indicating the presence of multiple inhibitory mechanisms against sarcomagenesis in chondrocytes. The inflammatory processes induced by mechanical injury and chondrocyte death through the release of danger-associated molecular patterns (DAMPs) are involved in the pathogenesis of posttraumatic osteoarthritis. The overexpression of BCLXL increases bone volume with a normal structure and maintains bone during aging by inhibiting osteoblast apoptosis. p53 inhibits osteoblast proliferation and enhances osteoblast apoptosis, thereby reducing bone formation, but also exerts positive effects on osteoblast differentiation through the Akt–FoxOs pathway. Apoptotic osteocytes release ATP, which induces the receptor activator of nuclear factor κ-B ligand (Rankl) expression and osteoclastogenesis, from pannexin 1 channels. Osteocyte death ultimately results in necrosis; DAMPs are released to the bone surface and promote the production of proinflammatory cytokines, which induce Rankl expression, and osteoclastogenesis is further enhanced. View Full-Text
Keywords: osteoarthritis; p53; Rb; ATP; DAMPs; Rankl; BCLXL; FoxO; osteoarthritis; apoptosis; necrosis osteoarthritis; p53; Rb; ATP; DAMPs; Rankl; BCLXL; FoxO; osteoarthritis; apoptosis; necrosis
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MDPI and ACS Style

Komori, T. Cell Death in Chondrocytes, Osteoblasts, and Osteocytes. Int. J. Mol. Sci. 2016, 17, 2045. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17122045

AMA Style

Komori T. Cell Death in Chondrocytes, Osteoblasts, and Osteocytes. International Journal of Molecular Sciences. 2016; 17(12):2045. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17122045

Chicago/Turabian Style

Komori, Toshihisa. 2016. "Cell Death in Chondrocytes, Osteoblasts, and Osteocytes" International Journal of Molecular Sciences 17, no. 12: 2045. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17122045

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