pubmed-article:18410228 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0044602 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0285761 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C1368105 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C1451005 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C1705325 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0029418 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0042866 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0042890 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0164786 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C0812228 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C1150481 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:18410228 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
pubmed-article:18410228 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:18410228 | pubmed:dateCreated | 2008-7-16 | lld:pubmed |
pubmed-article:18410228 | pubmed:abstractText | Osteoblast apoptosis plays a crucial role in bone remodeling. Physiological doses of 1 alpha,25(OH)(2)-vitamin D(3) (1,25D) protect osteoblasts against apoptosis by means of mechanisms only partially understood. We studied activation of an Akt survival cascade downstream of 1,25D nongenomic stimulation of phosphatidylinositide-3'-kinase (PI3K) in osteoblastic cells. We measured a dose- and time-dependent 1,25D induction of Akt phosphorylation (p-Akt) in cultured osteoblastic cells. Maximal response was achieved with 10 nM 1,25D after 5 min. We found that staurosporine (STSP)-induced apoptosis was significantly reduced in 1,25D-pretreated osteoblasts. 1,25D prosurvival effects were abolished when cells were preincubated with inhibitors of PI3K activation. By means of siRNA silencing, we proved that 1,25D induction of p-Akt requires a classic vitamin D receptor (VDR) in osteoblasts. Furthermore, non-osteoblastic CV-1 cells transfected with an enhanced green fluorescent protein (EGFP)-VDR construct responded to 1,25D treatment with a rapid p-Akt response associated with increased cell survival not detected in native, nontransfected cells. We measured increased levels of p-Akt substrates p-Bad and p-FKHR and significantly reduced activity of caspases 8 and 3/7 after 1,25D treatment. In addition, 1,25D-induced protection against apoptosis was abolished when osteoblasts were preincubated with pertussis toxin. We conclude that anti-apoptotic effects of 1,25D in osteoblasts occur through nongenomic activation of a VDR/PI3K/Akt survival pathway that includes phosphorylation of multiple p-Akt substrates and reduction of caspase activities. | lld:pubmed |
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pubmed-article:18410228 | pubmed:language | eng | lld:pubmed |
pubmed-article:18410228 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18410228 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:18410228 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18410228 | pubmed:month | Aug | lld:pubmed |
pubmed-article:18410228 | pubmed:issn | 1523-4681 | lld:pubmed |
pubmed-article:18410228 | pubmed:author | pubmed-author:ZanelloLaura... | lld:pubmed |
pubmed-article:18410228 | pubmed:author | pubmed-author:ZhangXiaoyuX | lld:pubmed |
pubmed-article:18410228 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18410228 | pubmed:volume | 23 | lld:pubmed |
pubmed-article:18410228 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18410228 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18410228 | pubmed:pagination | 1238-48 | lld:pubmed |
pubmed-article:18410228 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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