Source:http://linkedlifedata.com/resource/pubmed/id/19441105
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
2009-7-2
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| pubmed:abstractText |
It is unknown whether transforming growth factor beta1 (TGF-beta1) signaling uniformly participates in fibrogenic chronic liver diseases, irrespective of the underlying origin, or if other cytokines such as interleukin (IL)-13 share in fibrogenesis (e.g., due to regulatory effects on type I pro-collagen expression). TGF-beta1 signaling events were scored in 396 liver tissue samples from patients with diverse chronic liver diseases, including hepatitis B virus (HBV), hepatitis C virus (HCV), Schistosoma japonicum infection, and steatosis/steatohepatitis. Phospho-Smad2 staining correlated significantly with fibrotic stage in patients with HBV infection (n = 112, P < 0.001) and steatosis/steatohepatitis (n = 120, P < 0.01), but not in patients with HCV infection (n = 77, P > 0.05). In tissue with HBx protein expression, phospho-Smad2 was detectable, suggesting a functional link between viral protein expression and TGF-beta1 signaling. For IL-13, immunostaining correlated with fibrotic stage in patients with HCV infection and steatosis/steatohepatitis. IL-13 protein was more abundant in liver tissue lysates from three HCV patients compared with controls, as were IL-13 serum levels in 68 patients with chronic HCV infection compared with 20 healthy volunteers (72.87 +/- 26.38 versus 45.41 +/- 3.73, P < 0.001). Immunohistochemistry results suggest that IL-13-mediated liver fibrogenesis may take place in the absence of phospho-signal transducer and activator of transcription protein 6 signaling. In a subgroup of patients with advanced liver fibrosis (stage > or =3), neither TGF-beta nor IL-13 signaling was detectable. Conclusion: Depending on the cause of liver damage, a predominance of TGF-beta or IL-13 signaling is found. TGF-beta1 predominance is detected in HBV-related liver fibrogenesis and IL-13 predominance in chronic HCV infection. In some instances, the underlying fibrogenic mediator remains enigmatic.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
1527-3350
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| pubmed:author |
pubmed-author:BohleRainer MRM,
pubmed-author:ChenJia-LinJL,
pubmed-author:DooleyStevenS,
pubmed-author:GigouMichelleM,
pubmed-author:GodoyPatricioP,
pubmed-author:HuJun-HuaJH,
pubmed-author:HuangTongT,
pubmed-author:LammertFrankF,
pubmed-author:LiuYanY,
pubmed-author:MarxAlexanderA,
pubmed-author:MertensPeter RPR,
pubmed-author:MuellerSebastianS,
pubmed-author:SamuelDidierD,
pubmed-author:SeitzHelmut KHK,
pubmed-author:SingerManfred VMV,
pubmed-author:StickelFelixF,
pubmed-author:WengHong-LeiHL,
pubmed-author:XuLi-JunLJ,
pubmed-author:ZhouChengC,
pubmed-author:ZimmerVincentV
|
| pubmed:issnType |
Electronic
|
| pubmed:volume |
50
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
230-43
|
| pubmed:meshHeading | |
| pubmed:year |
2009
|
| pubmed:articleTitle |
The etiology of liver damage imparts cytokines transforming growth factor beta1 or interleukin-13 as driving forces in fibrogenesis.
|
| pubmed:affiliation |
Molecular Alcohol Research in Gastroenterology, Department of Medicine II, Faculty of Medicine at Mannheim, University of Heidelberg, Germany. honglei.weng@medma.uni-heidelberg.de
|
| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|