| pubmed-article:8589348 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0022801 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0677626 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C1522240 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:8589348 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:8589348 | pubmed:dateCreated | 1996-3-25 | lld:pubmed |
| pubmed-article:8589348 | pubmed:abstractText | The metabolic changes in a rat hepatoma cell line, AH70 cells, after co-culture with rat Kupffer cells (KC) were visualized and analysed using a fluorescence microscope equipped with a silicon intensified target camera and a laser scanning confocal microscopic system. Kupffer cells were isolated from male Wistar rats, and cultured without any stimuli. The non-activated KC reduced the mitochondrial energization in the cocultured AH70 cells within 2 h, which was indicated by decreased rhodamine 123 (Rh123) fluorescence. Either NG-monomethyl-L-arginine or dexamethasone significantly attenuated the KC-induced mitochondrial dysfunction in AH70 cells, suggesting the involvement of nitric oxide (NO) derived from inducible-type nitric oxide synthase (iNOS). Administration of monoclonal antibody (mAb) directed against rat ICAM-1 also prevented the decrease in Rh123 fluorescence. Electron microscopy revealed that the membrane-to-membrane attachment between KC and AH70 cells occurred within 2 h. A laser scanning confocal microscopic observation using mAb against ICAM-1 presented that the ICAM-1 expression on AH70 cells and KC increased after the co-culture. It is therefore concluded that the KC-mediated mitochondrial dysfunction of hepatoma cells largely depends on NO production by iNOS. Furthermore, the present study supports a scenario that the NO production and release from KC is triggered by the close contact with hepatoma cells through adhesion molecules such as ICAM-1. | lld:pubmed |
| pubmed-article:8589348 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8589348 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8589348 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8589348 | pubmed:issn | 0815-9319 | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:KatoSS | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:MiuraSS | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:SaitoHH | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:IshiiHH | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:HiguchiHH | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:KuroseII | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:YoneiYY | lld:pubmed |
| pubmed-article:8589348 | pubmed:author | pubmed-author:EbinumaHH | lld:pubmed |
| pubmed-article:8589348 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8589348 | pubmed:volume | 10 Suppl 1 | lld:pubmed |
| pubmed-article:8589348 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8589348 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8589348 | pubmed:pagination | S68-71 | lld:pubmed |
| pubmed-article:8589348 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:8589348 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:8589348 | pubmed:articleTitle | Nitric oxide mediates mitochondrial dysfunction in hepatoma cells induced by non-activated Kupffer cells: evidence implicating ICAM-1-dependent process. | lld:pubmed |
| pubmed-article:8589348 | pubmed:affiliation | Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan. | lld:pubmed |
| pubmed-article:8589348 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8589348 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8589348 | lld:pubmed |
