pubmed-article:14995074 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C0815000 | lld:lifeskim |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C1332817 | lld:lifeskim |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C1332823 | lld:lifeskim |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:14995074 | lifeskim:mentions | umls-concept:C2346501 | lld:lifeskim |
pubmed-article:14995074 | pubmed:dateCreated | 2004-3-3 | lld:pubmed |
pubmed-article:14995074 | pubmed:abstractText | Human neuroblastoma SK-N-SH cells strongly express CXC-chemokine receptor 4 (CXCR4), the principal coreceptor for X4 HIV-1 strains, and its natural ligand stromal cell-derived factor 1 (SDF-1, recently renamed CXCL12). We investigated the impact of CXCR4 blockade by the specific CXCR4 antagonist AMD3100 or by X4 HIV-1 virus particles on the growth and survival of neuroblastoma SK-N-SH cells. SK-N-SH cell proliferation was inhibited byAMD3100 and anti-CXCL12 neutralizing antibodies, but enhanced by exogenously added CXCL12. Upon prolongedexposure to AMD3100, SK-N-SH cell death occurred throughdeficit of survival-promoting and growth-stimulatory signals generated by endogenous CXCL12. In analogy with the observations made with the CXCR4 inhibitor AMD3100, the X4 HIV-1 strains IIIB and SF-2, but not the R5 strain BaL, caused a marked cytopathic effect and strongly effected SK-N-SH cell death after at least 10 days of incubation. However, no virus production could be detected in the HIV-1-inoculated SK-N-SH cell cultures. Exogenously added CXCL12 afforded partial protection against X4 HIV-1-induced cytopathicity in SK-N-SH cells. Our data indicate that the endogenous CXCL12/CXCR4 signaling axis is critical for neuroblastoma cell survival and proliferation. Long-term blockade of CXCR4 through physical contact with the X4 HIV-1 envelope can cause neuronal cell death. This mechanism may possibly play a role in X4 HIV-associated neurodegeneration. | lld:pubmed |
pubmed-article:14995074 | pubmed:language | eng | lld:pubmed |
pubmed-article:14995074 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14995074 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:14995074 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14995074 | pubmed:issn | 0145-5680 | lld:pubmed |
pubmed-article:14995074 | pubmed:author | pubmed-author:de ClercqEE | lld:pubmed |
pubmed-article:14995074 | pubmed:author | pubmed-author:ScholeJJ | lld:pubmed |
pubmed-article:14995074 | pubmed:author | pubmed-author:BridgesDD | lld:pubmed |
pubmed-article:14995074 | pubmed:author | pubmed-author:HatseSS | lld:pubmed |
pubmed-article:14995074 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14995074 | pubmed:volume | 49 Online Pub | lld:pubmed |
pubmed-article:14995074 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14995074 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14995074 | pubmed:pagination | OL443-52 | lld:pubmed |
pubmed-article:14995074 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:14995074 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:14995074 | pubmed:articleTitle | X4 HIV-1 induces neuroblastoma cell death by interference with CXCL12/CXCR4 interaction. | lld:pubmed |
pubmed-article:14995074 | pubmed:affiliation | Laboratory of Virology and Chemotherapy, Rega Institute for Medical Research, Katholieke Universiteit Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium. Sigrid.hatse@rega.kuleuven.ac.be | lld:pubmed |
pubmed-article:14995074 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:14995074 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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