| pubmed-article:11507096 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11507096 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:11507096 | lifeskim:mentions | umls-concept:C0005390 | lld:lifeskim |
| pubmed-article:11507096 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:11507096 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:11507096 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:11507096 | lifeskim:mentions | umls-concept:C0086355 | lld:lifeskim |
| pubmed-article:11507096 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:11507096 | pubmed:issue | 42 | lld:pubmed |
| pubmed-article:11507096 | pubmed:dateCreated | 2001-10-15 | lld:pubmed |
| pubmed-article:11507096 | pubmed:abstractText | Toxic bile salts induce hepatocyte apoptosis by both Fas-dependent and -independent mechanisms. In this study, we examined the cellular mechanisms responsible for Fas-independent, bile acid-mediated apoptosis. HuH-7 cells, which are known to be Fas deficient, were stably transfected with the sodium-dependent bile acid transporting polypeptide. The toxic bile acid glycochenodeoxycholate (GCDC)-induced apoptosis in these cells in a time- and concentration-dependent manner. Apoptosis and mitochondrial cytochrome c release were inhibited by transfection with dominant negative FADD, CrmA transfection, or treatment with the selective caspase 8 inhibitor IETD-CHO. These observations suggested the Fas-independent apoptosis was also death receptor mediated. Reverse transcriptase-polymerase chain reaction demonstrated tumor necrosis factor-R1, tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-R1/DR4, -R2/DR5, and TRAIL, but not tumor necrosis factor-alpha expression by these cells. GCDC treatment increased expression of TRAIL-R2/DR5 mRNA and protein 10-fold while expression of TRAIL-R1 was unchanged. Furthermore, aggregation of TRAIL-R2/DR5, but not TRAIL-R1/DR4 was observed following GCDC treatment of the cells. Induction of TRAIL-R2/DR5 expression and apoptosis by bile acids provides new insights into the mechanisms of hepatocyte apoptosis and the regulation of TRAIL-R2/DR5 expression. | lld:pubmed |
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| pubmed-article:11507096 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11507096 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11507096 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11507096 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11507096 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11507096 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:11507096 | pubmed:author | pubmed-author:HiguchiHH | lld:pubmed |
| pubmed-article:11507096 | pubmed:author | pubmed-author:GoresG JGJ | lld:pubmed |
| pubmed-article:11507096 | pubmed:author | pubmed-author:BronkS FSF | lld:pubmed |
| pubmed-article:11507096 | pubmed:author | pubmed-author:TakikawaYY | lld:pubmed |
| pubmed-article:11507096 | pubmed:author | pubmed-author:TakimotoRR | lld:pubmed |
| pubmed-article:11507096 | pubmed:author | pubmed-author:El-DeiryWW | lld:pubmed |
| pubmed-article:11507096 | pubmed:author | pubmed-author:WerneburgNN | lld:pubmed |
| pubmed-article:11507096 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11507096 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:11507096 | pubmed:volume | 276 | lld:pubmed |
| pubmed-article:11507096 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11507096 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11507096 | pubmed:pagination | 38610-8 | lld:pubmed |
| pubmed-article:11507096 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:11507096 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11507096 | pubmed:articleTitle | The bile acid glycochenodeoxycholate induces trail-receptor 2/DR5 expression and apoptosis. | lld:pubmed |
| pubmed-article:11507096 | pubmed:affiliation | Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905, USA. | lld:pubmed |
| pubmed-article:11507096 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11507096 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11507096 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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