BMP-2 prevents apoptosis of the N1511 chondrocytic cell line through PI3K/Akt-mediated NF-κB activation
Journal of Bone and Mineral Metabolism, ISSN: 0914-8779, Vol: 23, Issue: 6, Page: 411-419
2005
- 57Citations
- 25Captures
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Metrics Details
- Citations57
- Citation Indexes57
- 57
- CrossRef45
- Captures25
- Readers25
- 25
Article Description
The signal transduction pathway by which bone morphogenetic protein-2 (BMP-2) regulates apoptosis in chondrocytes remains largely unknown. We investigated the involvement of phosphatidylinositol 3-kinase (PI3K)/Akt-mediated NF-κB activation by BMP-2 stimulation in the modulation of this antiapoptotic process in a chondrocytic cell line, N1511. BMP-2 prevented apoptosis through the inhibition of caspase-3 and -9 and an increase in Bcl-xL expression, and this antiapoptotic effect was inhibited by Noggin. Not only was NF-κB p65 activated transiently in the early phase (5-15 min) after treatment with BMP-2 but p65 at serine 536 was phosphorylated from 5 min as well. Akt was rapidly phosphorylated in response to BMP-2 treatment; however, the inhibition of PI3K by Wortmannin markedly reduced the phosphorylation of Akt by BMP-2. Wortmannin also decreased the NF-κB transcriptional activity that was up-regulated by BMP-2. Thus, BMP-2-induced NF-κB activation is mediated by PI3K/Akt signaling. Wortmannin treatment inhibited the antiapoptotic effect of BMP-2. These data indicate that BMP-2 can utilize a new signal transduction pathway in the NF-κB activation system, which plays a crucial role in the survival of the N1511 chondrocytic cell line. © Springer-Verlag 2005.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=27644484777&origin=inward; http://dx.doi.org/10.1007/s00774-005-0622-7; http://www.ncbi.nlm.nih.gov/pubmed/16261446; http://link.springer.com/10.1007/s00774-005-0622-7; http://www.springerlink.com/index/10.1007/s00774-005-0622-7; http://www.springerlink.com/index/pdf/10.1007/s00774-005-0622-7; https://dx.doi.org/10.1007/s00774-005-0622-7; https://link.springer.com/article/10.1007/s00774-005-0622-7
Springer Science and Business Media LLC
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