Interferon-gamma acts proapoptotic on Hepatic Stellate Cells (HSC) and abrogates the antiapoptotic Effect of Interferon-alpha by an HSP70 dependant Pathway

Saile, Bernhard; Eisenbach, Christoph; Dudas, J.; Ramadori, Giuliano

doi:10.1055/s-2005-861581

Cited by 8 publications

(10 citation statements)

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“…Furthermore, it was shown that IFNγ acts pro-apoptotic on hepatic stellate cells 33. Hepatic stellate cells, especially myofibroblasts, are considered as major fibrogenic cell population in chronic liver disease and may also be involved in the initial phase of fibrosis in Abcb −/− mice 13 34.…”

Section: Discussionmentioning

confidence: 99%

Bone marrow transplantation improves hepatic fibrosis inAbcb4^−/−mice via Th1 response and matrix metalloproteinase activity

Roderfeld

Räth

Pasupuleti

et al. 2011

Gut

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Section: Discussionmentioning

confidence: 99%

Bone marrow transplantation improves hepatic fibrosis inAbcb4^−/−mice via Th1 response and matrix metalloproteinase activity

Roderfeld

Räth

Pasupuleti

et al. 2011

Gut

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“…Several cytokines can induce HSC apoptosis. For example, INF‐γ successfully blocks HSC proliferation and induces HSC apoptosis 16 . Tumor necrosis factor‐α also has an antiproliferative effect on HSC and induces HSC apoptosis in the presence of cycloheximide, an inhibitor of protein synthesis 17,18 .…”

Section: Successful Treatment Of the Underlying Etiology Reverses Fibmentioning

confidence: 99%

Hepatic stellate cells and the reversal of fibrosis

Kisseleva

Brenner

2006

J of Gastro and Hepatol

238

193

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Hepatic fibrosis is an outcome of many chronic liver diseases, such as viral and autoimmune hepatitis, and of alcohol consumption and biliary obstruction. Prolonged liver injury results in hepatocyte damage, which triggers activation of hepatic stellate cells (HSC) and recruitment of inflammatory cells into the liver. The HSC play a critical role in fibrogenesis. They produce collagen type I and secrete pro-fibrogenic cytokines and inhibitors of matrix-degrading enzymes (tissue inhibitor of matrix metalloproteinase), causing the production of extracellular matrix deposition over degradation. However, many clinical and experimental studies suggest that this process can be reversed, including the apoptosis of activated HSC. Thus, HSC represent an appealing target for antifibrotic therapy. This review will focus on some aspects of etiology and molecular pathogenesis of liver fibrosis and the reversal of fibrosis.

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“…Furthermore, in vitro studies have classiWed SMA/ Fibulin-2/IL-6 positive cells as MF (Knittel et al 1999a;Ramadori and Saile 2002;Saile et al 2002). Functional in vitro studies suggest that cultured rat HSC and MF diVer not only in expressing diVerent markers, but also in expressing diVerent cytokines and growth factors (Schirmacher et al 1992;Tiggelman et al 1995;Knittel et al 1999a), as well as their diVerent responses to various cytokines and growth factors (Tiggelman et al 1995;Saile et al 2002Saile et al , 2004. Moreover, they also diVer in apoptotic and proliferation characteristics, and in cell cycle regulation Dudas et al 2003;Ogawa et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Thy-1 is expressed in myofibroblasts but not found in hepatic stellate cells following liver injury

Dudás

Mansuroglu

Batusic

et al. 2008

Histochem Cell Biol

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Thy-1 (CD90) is an adhesion molecule induced in Wbroblast populations associated with wound healing and Wbrosis. In this study the question whether Thy-1-geneexpression can be induced in hepatic stellate cells (HSC) in vivo, under conditions of liver injury or liver regeneration was addressed. Acute and chronic rat liver injury was induced by the administration of CCl 4 . For comparison, cirrhotic human liver, and rat 67% partial hepatectomy (PH) was studied as well. Thy-1-gene-expression was examined also in isolated human liver myoWbroblasts. Thy-1-mRNA expression was signiWcantly upregulated in chronic liver injury. Thy-1 + cells were detected in the periportal area of rat liver specimens in normal-, injured-and regenerativeconditions. In chronic human and rat liver injury, Thy-1 + cells were located predominantly in scar tissue. In the pericentral necrotic zone after CCl 4 -treatment, no induction of Thy-1 was found. Gremlin and Thy-1 showed comparable localization in the periportal areas. Thy-1 was not detected in either normal or capillarized sinusoids, in isolated rat HSC, and was neither inducible by inXammatory cytokines in isolated HSC, nor upregulated in treated myoWbroblasts. Based upon these data Thy-1 is not a marker of "activated" sinusoidal HSC, but it is a marker of "activated" (myo)Wbroblasts found in portal areas and in scar tissue.

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Interferon-gamma acts proapoptotic on Hepatic Stellate Cells (HSC) and abrogates the antiapoptotic Effect of Interferon-alpha by an HSP70 dependant Pathway

Cited by 8 publications

References 0 publications

Bone marrow transplantation improves hepatic fibrosis inAbcb4^−/−mice via Th1 response and matrix metalloproteinase activity

Bone marrow transplantation improves hepatic fibrosis inAbcb4^−/−mice via Th1 response and matrix metalloproteinase activity

Hepatic stellate cells and the reversal of fibrosis

Thy-1 is expressed in myofibroblasts but not found in hepatic stellate cells following liver injury

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Interferon-gamma acts proapoptotic on Hepatic Stellate Cells (HSC) and abrogates the antiapoptotic Effect of Interferon-alpha by an HSP70 dependant Pathway

Cited by 8 publications

References 0 publications

Bone marrow transplantation improves hepatic fibrosis inAbcb4−/−mice via Th1 response and matrix metalloproteinase activity

Bone marrow transplantation improves hepatic fibrosis inAbcb4−/−mice via Th1 response and matrix metalloproteinase activity

Hepatic stellate cells and the reversal of fibrosis

Thy-1 is expressed in myofibroblasts but not found in hepatic stellate cells following liver injury

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Resources

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Bone marrow transplantation improves hepatic fibrosis inAbcb4^−/−mice via Th1 response and matrix metalloproteinase activity

Bone marrow transplantation improves hepatic fibrosis inAbcb4^−/−mice via Th1 response and matrix metalloproteinase activity