| pubmed-article:18973553 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18973553 | lifeskim:mentions | umls-concept:C0001849 | lld:lifeskim |
| pubmed-article:18973553 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:18973553 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:18973553 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18973553 | pubmed:dateCreated | 2008-10-31 | lld:pubmed |
| pubmed-article:18973553 | pubmed:abstractText | Platelet-derived growth factor (PDGF) has been implicated in promoting survival and proliferation of immature neurons, and even protecting neurons from gp120-induced cytotoxicity. However, the mechanisms involved in neuroprotection are not well understood. In the present study we demonstrate the role of phosphatidylinositol 3-kinase (PI3K)/Akt signaling in PDGF-mediated neuroprotection. Pharmacological inhibition of PI3K greatly reduced the ability of PDGF-BB to block gp120 IIIB-mediated apoptosis and cell death in human neuroblastoma cells. The role of Akt in PDGF-mediated protection was further corroborated using a dominant-negative mutant of Akt, which was able to block the protective effect of PDGF. We next sequentially examined the signals downstream of Akt in PDGF-mediated protection in human neuroblastoma cells. In cells pretreated with PDGF prior to gp120 there was increased phosphorylation of both GSK-3beta and Bad, an effect that was inhibited by PI3-kinase inhibitor. Nuclear translocation of NF-kappaB, which lies downstream of GSK-3beta, however, remained unaffected in cells treated with PDGF. In addition to inducing phosphorylation of Bad, PDGF-mediated protection also involved down-regulation of the proapoptotic protein Bax. Furthermore, PDGF-mediated protection also involved the inhibition of gp120-induced release of mitochondrial cytochrome C. Our findings thus underscore the roles of both PI3K/Akt and Bcl family pathways in PDGF-mediated neuroprotection. | lld:pubmed |
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| pubmed-article:18973553 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18973553 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18973553 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18973553 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18973553 | pubmed:issn | 1460-9568 | lld:pubmed |
| pubmed-article:18973553 | pubmed:author | pubmed-author:ZhuXuhuiX | lld:pubmed |
| pubmed-article:18973553 | pubmed:author | pubmed-author:BuchShilpaS | lld:pubmed |
| pubmed-article:18973553 | pubmed:author | pubmed-author:WilliamsRache... | lld:pubmed |
| pubmed-article:18973553 | pubmed:author | pubmed-author:DhillonNavnee... | lld:pubmed |
| pubmed-article:18973553 | pubmed:author | pubmed-author:YaoHonghongH | lld:pubmed |
| pubmed-article:18973553 | pubmed:author | pubmed-author:PengFuwangF | lld:pubmed |
| pubmed-article:18973553 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18973553 | pubmed:volume | 28 | lld:pubmed |
| pubmed-article:18973553 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18973553 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18973553 | pubmed:pagination | 1255-64 | lld:pubmed |
