Hepatic stellate cells display a functional vascular smooth muscle cell phenotype in a three-dimensional co-culture model with endothelial cells

Wirz, W.; Antoine, Marianne; Tag, Carmen G.; Gressner, A. M.; Korff, Thomas; Hellerbrand, Claus; Kiefer, Paul

doi:10.1111/j.1432-0436.2007.00260.x

Cited by 65 publications

(47 citation statements)

References 33 publications

(68 reference statements)

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“…The former cells lack growth ability and spontaneously undergo activation (induction of SMA expression) and, as recently described, to terminal diVerentiation characterized by expression of a large panel of late vascular smooth muscle cell markers (Wirz et al 2008) and manifested by the spontaneous Fasmediated apoptosis . Importantly, these same investigators have (Ogawa et al 2007;Saile et al 2002;Dudas et al 2003), clearly demonstrated that the minor cell population, MFs, but not aHSCs, have replicative activity (Table 2).…”

Section: Discussionmentioning

confidence: 67%

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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Section: Discussionmentioning

confidence: 67%

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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“…Concurrently, activated HSCs cultured with SECs expressed functional smooth muscle cell phenotype and formed capillary-like structures in angiogenesis assays. Taking into consideration that tumours activate HSCs, their contribution to neoangiogenesis through interactions with SECs was implicated in these studies [114,167] .…”

Section: Hepatic Stellate Cellsmentioning

confidence: 99%

Natural history of hepatic metastases from colorectal cancer - pathobiological pathways with clinical significance

Paschos

Majeed

Bird

2014

WJG

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Colorectal cancer hepatic metastases represent the final stage of a multi-step biological process. This process starts with a series of mutations in colonic epithelial cells, continues with their detachment from the large intestine, dissemination through the blood and/or lymphatic circulation, attachment to the hepatic sinusoids and interactions with the sinusoidal cells, such as sinusoidal endothelial cells, Kupffer cells, stellate cells and pit cells. The metastatic sequence terminates with colorectal cancer cell invasion, adaptation and colonisation of the hepatic parenchyma. All these events, termed the colorectal cancer invasion-metastasis cascade, include multiple molecular pathways, intercellular interactions and expression of a plethora of chemokines and growth factors, and adhesion molecules, such as the selectins, the integrins or the cadherins, as well as enzymes including matrix metalloproteinases. This review aims to present recent advances that provide insights into these cell-biological events and emphasizes those that may be amenable to therapeutic targeting. Paschos KA, Majeed AW, Bird NC. Natural history of hepatic metastases from colorectal cancer -pathobiological pathways with clinical significance.

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“…Activated HSCs and myofibroblasts directly govern hepatocarcinogenesis in a TGF-ß dependent fashion by inducing autocrine TGF-ß signaling and nuclear ß-catenin accumulation in neoplastic hepatocytes (Mikula et al, 2006). Activated HSCs not only promote tumor progression by affecting ECM remodeling but also secrete angiopoietin that induces angiogenesis (Théret et al, 2001;Taura et al, 2008, Wirz et al, 2008. Vascular endothelial growth factor (VEGF) was detected in hepatoma cells and HSCs, and increased VEGF expression was associated with tumor progression in HCC (Torimura et al, 1998).…”

Section: Role Of Hsc In Hcc Developmentmentioning

confidence: 99%

Hepatic Stellate Cells in Inflammation‐Fibrosis‐Carcinoma Axis

Wang

Cheng

Gao

et al. 2010

The Anatomical Record

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Almost 80% of hepatocellular carcinoma (HCC) cases are associated with chronic hepatitis and cirrhosis resulting from inflammation and fibrosis. A three-step process of ''inflammation-fibrosis-carcinoma'' is believed to be involved in hepatocarcinogenesis. The activation of hepatic stellate cells (HSCs) may serve as an important mediator in the process of inflammation-fibrosis-carcinoma axis, even in tumor metastasis. A remarkable knowledge of activated HSCs in the pathology of HCC development is mostly focused on the liver fibrosis. The molecular links that connects inflammation and cancer in the activation of HSC are not completely known. This highlights urgent need to increase our understanding of the cellular and molecular mechanisms, by which activation of HSCs is involved in the hepatic inflammation, carcinogenesis, and metastasis.

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Hepatic stellate cells display a functional vascular smooth muscle cell phenotype in a three-dimensional co-culture model with endothelial cells

Cited by 65 publications

References 33 publications

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

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

Natural history of hepatic metastases from colorectal cancer - pathobiological pathways with clinical significance

Hepatic Stellate Cells in Inflammation‐Fibrosis‐Carcinoma Axis

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