Ethanol and Arachidonic Acid Increase α2(I) Collagen Expression in Rat Hepatic Stellate Cells Overexpressing Cytochrome P450 2E1

Nieto, Natalia; Greenwel, Patricia; Friedman, Scott L.; Zhang, Fan; Dannenberg, Andrew J.; Cederbaum, Arthur I.

doi:10.1074/jbc.m001422200

Cited by 118 publications

(121 citation statements)

References 60 publications

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“…The maximal induction of COX-2 protein in HSC-T6 given B16M-CM under normoxic conditions was observed after 18 hours (2.5-fold over basal level; data not shown). COX-2 activity in HSC-T6 cells, measured as PGE2 production, 26 also increased in response to B16M-CM and hypoxia (Fig. 9C).…”

Section: Proangiogenic Response Of Hepatic Stellate Cells To Melanomamentioning

confidence: 94%

Proangiogenic Role of Tumor–Activated Hepatic Stellate Cells in Experimental Melanoma Metastasis

2003

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Myofibroblasts infiltrate malignant liver tumors, although their pathogenic implications are unclear. Immunohistochemical detection of ␣-smooth muscle actin, glial fibrillary acidic protein (GFAP), and CD31 and CD34 expression was used to analyze the contribution of myofibroblasts to angiogenesis in hepatic metastasis produced by intrasplenically-injected B16 melanoma (B16M). Because activated hepatic stellate cells (HSCs) are oxygen-sensing myofibroblasts producing vascular endothelial growth factor (VEGF), the effect of B16M and human A375 melanoma supernatants on VEGF production by immortalized rat HSC line T6 and primary cultured human HSCs also was studied under an hypoxic atmosphere mimicking a tumor microenvironment. Myofibroblast infiltration preceded endothelium recruitment in avascular micrometastasis and generated specific stroma for sinusoidal-type and portal-type angiogeneses. Thereafter, myofibroblasts and endothelial cells colocalized within both angiogenic patterns and their numerical densities correlated with metastasis development. Myofibroblasts often were GFAPpositive, suggesting an HSC origin. Melanoma supernatants stimulated VEGF messenger RNA and protein synthesis by HSCs. These effects were potentiated by hypoxia. VEGF up-regulation was accompanied by increased expression of cyclooxygenase type 2 (COX-2) and PGE2 synthesis. HSC production of VEGF decreased under COX-2 inhibition, whereas it was increased by exogenous PGE2. The high VEGF expression in HSCs induced by melanoma factors and hypoxia resulted in mitogenic, antiapoptotic, and motogenic stimulation of both murine hepatic sinusoidal endothelium and human umbilical vein endothelium. In conclusion, temporal and positional relationships evolve between myofibroblast and endothelium recruitment during metastasis development. Mechanistically, hypoxic induction of VEGF in tumor-activated HSCs may create a proangiogenic microenvironment, facilitating endothelial cell recruitment and survival during hepatic metastasis transition from an avascular to a vascular stage. (HEPATOLOGY 2003;37:674-685.)

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Section: Proangiogenic Response Of Hepatic Stellate Cells To Melanomamentioning

confidence: 94%

Proangiogenic Role of Tumor–Activated Hepatic Stellate Cells in Experimental Melanoma Metastasis

2003

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“…CYP2E1 is an important source of reactive oxygen species (ROS) in alcohol-induced injury and fibrosis, generating superoxide (O 2 -) and hydrogen peroxide (H 2 O 2 ). It has been detected that inhibition of CYP2E1 activity by diallylsulfide (DAS) prevents induction of collagen I gene expression in rat stellate cells overexpressing CYP2E1 [15]. Oxidative stress also activates the c-Jun NH 2 -terminal kinase (JNK), a protein which regulates secretion of proinflammatory cytokines by cultured HSCs [16,17].…”

Section: Introductionmentioning

confidence: 99%

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

Szuster‐Ciesielska

Plewka

Daniluk

et al. 2009

Biochemical Pharmacology

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To cite this version:Agnieszka Szuster-Ciesielska, Krzysztof Plewka, Jadwiga Daniluk, Martyna Kandefer-Szerszeń. Zinc supplementation attenuates ethanol-and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling. Biochemical Pharmacology, Elsevier, 2009, 78 (3) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Parallel cotransfection with 25 ng/ml of the control pRL-null (Promega) containing the cDNA encoding for Renilla luciferase was performed to normalize for transfection efficiency. Cells were incubated in the presence of the transfection mix for 24 h, after which the media were replaced and the cells treated with 30 M AdoMet for 24 h. Samples for the CAT activity were collected, and the reaction was run using a kit from Promega as described previously (29).…”

Section: Methodsmentioning

confidence: 99%

“…On the other hand, the activity of the Ϫ772COL1A2-CAT vector was significantly lower. The Ϫ772 to Ϫ378 region of the human or mouse COL1A2 gene contains a silencer element (28,29,31). Addition of 30 M AdoMet for 24 h after transfection decreased the basal activity of both the Ϫ3500COL1A2-CAT and the Ϫ378COL1A2-CAT reporter vectors.…”

Section: Induction Of Liver Fibrosis In Mouse Col1a2 Promoter Transgementioning

confidence: 99%

“…Addition of 30 M AdoMet for 24 h after transfection decreased the basal activity of both the Ϫ3500COL1A2-CAT and the Ϫ378COL1A2-CAT reporter vectors. It is interesting that AdoMet lowered CAT activity in cells transfected with the Ϫ378COL1A2-CAT construct, which contains the Ϫ378 to ϩ58 bp region that is essential for increased basal COL1A2 expression and responsiveness to oxidative stress and cytokines such as TNF␣ and TGF␤ (11,12,21,29,32,37).…”

Section: Induction Of Liver Fibrosis In Mouse Col1a2 Promoter Transgementioning

confidence: 99%

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S-Adenosylmethionine Blocks Collagen I Production by Preventing Transforming Growth Factor-β Induction of the COL1A2 Promoter

Nieto

Cederbaum

2005

Journal of Biological Chemistry

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Ethanol and Arachidonic Acid Increase α2(I) Collagen Expression in Rat Hepatic Stellate Cells Overexpressing Cytochrome P450 2E1

Cited by 118 publications

References 60 publications

Proangiogenic Role of Tumor–Activated Hepatic Stellate Cells in Experimental Melanoma Metastasis

Proangiogenic Role of Tumor–Activated Hepatic Stellate Cells in Experimental Melanoma Metastasis

Zinc supplementation attenuates ethanol- and acetaldehyde-induced liver stellate cell activation by inhibiting reactive oxygen species (ROS) production and by influencing intracellular signaling

S-Adenosylmethionine Blocks Collagen I Production by Preventing Transforming Growth Factor-β Induction of the COL1A2 Promoter

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