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- W1500676217 abstract "Hepatic stellate cells (HSC), a pericyte-like nonparenchymal liver cell population, are regarded as the principal matrix-synthesizing cells of fibrotic liver. They might also play a role during liver inflammation. The present study analyzed (i) expression of cell adhesion molecules (CAMs) mediating cell infiltration, like intercellular adhesion molecule-1 (I-CAM-1) and vascular cell adhesion molecule-1 (V-CAM-1), by HSC, (ii) CAM regulation in HSC by growth factors and inflammatory cytokines, and (iii) CAM expression in situ during liver inflammation, using immunochemistry and Northern blot analysis. I-CAM-1 and V-CAM-1 expression was present in HSC in vitro and in cells located in the sinusoidal/perisinusoidal area of normal liver. Growth factors, eg, transforming growth factor-β1, down-regulated I-CAM-1- and V-CAM-1-coding mRNAs and stimulated N-CAM expression of HSC. In contrast, inflammatory cytokines like tumor necrosis factor-α reduced N-CAM-coding mRNAs, whereas induction of I-CAM-1- and V-CAM-1-specific transcripts increased severalfold. In situ, messengers specific for I-CAM-1 and V-CAM-1 were induced 3 hours after CCl4 treatment (thereby preceding mononuclear cell infiltration starting at 12 hours), were expressed at maximal levels 9–12 hours after CCl4 application, and decreased afterwards. I-CAM-1 and V-CAM-1 immunoreactivity increased in a linear fashion starting 3 hours after CCl4-induced liver injury, was detected in highest amounts at 24–48 hours characterized by maximal cell infiltration, and returned to baseline values at 96 hours. Interestingly, the induction/repression of CAM-specific messengers paralleled the time kinetics of tumor necrosis factor-α/transforming growth factor-β1 expression in injured liver. HSC might be important during the onset of hepatic tissue injury as proinflammatory elements and might interact with I-CAM-1 and V-CAM-1 ligand-bearing cells, namely lymphocyte function-associated antigen-1- or Mac-1/very late activation antigen-4-positive inflammatory cells, thereby modulating the recruitment and migration of mononuclear cells within the perisinusoidal space of diseased livers. Hepatic stellate cells (HSC), a pericyte-like nonparenchymal liver cell population, are regarded as the principal matrix-synthesizing cells of fibrotic liver. They might also play a role during liver inflammation. The present study analyzed (i) expression of cell adhesion molecules (CAMs) mediating cell infiltration, like intercellular adhesion molecule-1 (I-CAM-1) and vascular cell adhesion molecule-1 (V-CAM-1), by HSC, (ii) CAM regulation in HSC by growth factors and inflammatory cytokines, and (iii) CAM expression in situ during liver inflammation, using immunochemistry and Northern blot analysis. I-CAM-1 and V-CAM-1 expression was present in HSC in vitro and in cells located in the sinusoidal/perisinusoidal area of normal liver. Growth factors, eg, transforming growth factor-β1, down-regulated I-CAM-1- and V-CAM-1-coding mRNAs and stimulated N-CAM expression of HSC. In contrast, inflammatory cytokines like tumor necrosis factor-α reduced N-CAM-coding mRNAs, whereas induction of I-CAM-1- and V-CAM-1-specific transcripts increased severalfold. In situ, messengers specific for I-CAM-1 and V-CAM-1 were induced 3 hours after CCl4 treatment (thereby preceding mononuclear cell infiltration starting at 12 hours), were expressed at maximal levels 9–12 hours after CCl4 application, and decreased afterwards. I-CAM-1 and V-CAM-1 immunoreactivity increased in a linear fashion starting 3 hours after CCl4-induced liver injury, was detected in highest amounts at 24–48 hours characterized by maximal cell infiltration, and returned to baseline values at 96 hours. Interestingly, the induction/repression of CAM-specific messengers paralleled the time kinetics of tumor necrosis factor-α/transforming growth factor-β1 expression in injured liver. HSC might be important during the onset of hepatic tissue injury as proinflammatory elements and might interact with I-CAM-1 and V-CAM-1 ligand-bearing cells, namely lymphocyte function-associated antigen-1- or Mac-1/very late activation antigen-4-positive inflammatory cells, thereby modulating the recruitment and migration of mononuclear cells within the perisinusoidal space of diseased livers. Hepatic tissue repair reactions in response to liver injury are characterized by infiltration of the parenchyma by inflammatory cells, principally lymphocytes, granulocytes, and monocytes/macrophages. Infiltration is a multistep process comprising the so-called rolling followed by sticking of blood cells to the endothelial layer and transmigration through the hepatic endothelial lining into the tissue.1Imhof BA Dunon D Leukocyte migration and adhesion.Adv Immunol. 1995; 58: 345-416Crossref PubMed Google Scholar, 2Ley K Molecular mechanisms of leukocyte recruitment in the inflammatory process.Cardiovasc Res. 1996; 32: 733-742Crossref PubMed Scopus (319) Google Scholar, 3Butcher E Picker L Lymphocyte homing and homeostasis.Science. 1996; 272: 60-66Crossref PubMed Scopus (2517) Google Scholar The recruitment of specific leukocyte populations is mediated by chemokines and by the interaction of adhesion molecules on inflammatory cells and on endothelial cells on the other side.1Imhof BA Dunon D Leukocyte migration and adhesion.Adv Immunol. 1995; 58: 345-416Crossref PubMed Google Scholar, 2Ley K Molecular mechanisms of leukocyte recruitment in the inflammatory process.Cardiovasc Res. 1996; 32: 733-742Crossref PubMed Scopus (319) Google Scholar, 3Butcher E Picker L Lymphocyte homing and homeostasis.Science. 1996; 272: 60-66Crossref PubMed Scopus (2517) Google Scholar Recently some of the basic mechanisms responsible for the transmigration of leukocytes through the hepatic endothelial lining have been elucidated; however, the further migration and resulting accumulation of inflammatory cells in areas of liver damage are poorly characterized.4Jaeschke H Cellular adhesion molecules: regulation and functional significance in the pathogenesis of liver diseases.Am J Physiol. 1997; 273: G602-G611PubMed Google Scholar, 5Stamatoglou SC Hughes RC Cell adhesion molecules in liver function and pattern formation.FASEB J. 1994; 8: 420-427PubMed Google Scholar Hepatic stellate cells (HSC), also designated as Ito cells, fat storing cells, or lipocytes, play a major role in vitamin A metabolism and are presently regarded as the principal cell type responsible for matrix accumulation during liver repair reactions including fibrosis.6Pinzani M Novel insights into the biology and physiology of the Ito cell.Pharmacol Ther. 1995; 66: 387-412Crossref PubMed Scopus (162) Google Scholar, 7Hautekeete ML Geerts A The hepatic stellate (Ito) cell: its role in human liver disease.Virchows Arch. 1997; 430: 195-207Crossref PubMed Scopus (268) Google Scholar, 8Friedman SL Hepatic stellate cells.Prog Liver Dis. 1996; 14: 101-130PubMed Google Scholar HSC are situated in the space of Disse between the sinusoidal endothelium and hepatocytes and exhibit long cytoplasmic processes that underlie the endothelium and embrace the sinusoid but also have contact with hepatocytes. Because HSC reflect the cell population immediately contacting transmigrated leukocytes on one side and hepatocytes on the other side, they could play a role in the recruitment of inflammatory cells into the liver parenchyma and subsequently in their targeting to damaged hepatocytes. To address this question, the present study analyzed HSC with respect to the expression of cell adhesion molecules and their regulation by mediators involved in hepatic tissue repair reactions. Among cell adhesion molecules (CAMs) the report concentrates on intercellular cell adhesion molecule-1 (I-CAM-1) and vascular cell adhesion molecule-1 (V-CAM-1), because the I-CAM/ lymphocyte function associated antigen (LFA)-1 and V-CAM/very late activation antigen (VLA)-4 adhesion pathways have been described as fundamental for leukocyte recruitment at sites of inflammation.1Imhof BA Dunon D Leukocyte migration and adhesion.Adv Immunol. 1995; 58: 345-416Crossref PubMed Google Scholar, 2Ley K Molecular mechanisms of leukocyte recruitment in the inflammatory process.Cardiovasc Res. 1996; 32: 733-742Crossref PubMed Scopus (319) Google Scholar, 3Butcher E Picker L Lymphocyte homing and homeostasis.Science. 1996; 272: 60-66Crossref PubMed Scopus (2517) Google Scholar, 9Postigo A Teixido J Sanchez-Madrid F The α4β1/VCAM-1 adhesion pathway in physiology and disease.Res Immunol. 1993; 144: 723-735Crossref PubMed Scopus (88) Google Scholar, 10Patarroyo M Makgoba M Leucocyte adhesion to cell in immune and inflammatory responses.Lancet. 1989; II: 1139-1142Abstract Scopus (92) Google Scholar In addition, the regulation of neural cell adhesion molecule (N-CAM, also termed CD56) was analyzed because N-CAM, known to be expressed by HSC following activation, might be involved in the migration of CD56-positive lymphocytes or HSC and in the termination of HSC proliferation induced by tissue injury.11Palucka AK Porwit A Reizenstein P A supportive role of neural cell adhesion molecule (NCAM) in adhesion between leukaemic blasts and cytotoxic lymphocytes.Scand J Immunol. 1992; 35: 399-406Crossref PubMed Scopus (12) Google Scholar, 12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar Basic features of the response of HSC to hepatic tissue injury are phenotypical and functional changes, a process called activation.6Pinzani M Novel insights into the biology and physiology of the Ito cell.Pharmacol Ther. 1995; 66: 387-412Crossref PubMed Scopus (162) Google Scholar, 7Hautekeete ML Geerts A The hepatic stellate (Ito) cell: its role in human liver disease.Virchows Arch. 1997; 430: 195-207Crossref PubMed Scopus (268) Google Scholar, 8Friedman SL Hepatic stellate cells.Prog Liver Dis. 1996; 14: 101-130PubMed Google Scholar Activation includes HSC proliferation, transforming star-shaped cells rich in vitamin A to vitamin A-deficient cells of myofibroblast-like appearance (activated HSC) displaying contractile properties. Furthermore, activation is characterized by differential gene expression of connective tissue components, matrix-degrading enzymes, and their inhibitors, resulting in matrix accumulation colocalized with activated HSC. Interestingly, this in vivo activation process strongly resembles the morphological and functional changes observed in HSC during primary culture. Therefore HSC in vitro are commonly used as a model to study the role of these cells during hepatic tissue repair, which additionally offers the unique opportunity to study the functional role of these cells at different activation steps reflecting different phases of tissue injury. Because the potential involvement of HSC in leukocyte recruitment might be affected by their differentiation stage, the expression and regulation of CAMs was studied in HSC in vitro at different steps of activation. To clarify whether the data obtained from former in vitro studies are relevant to in vivo conditions, expression of I-CAM-1 and V-CAM-1 was analyzed in the carbon tetrachloride (CCl4) in vivo model for acute liver damage accompanied by hepatic inflammation. Using this model, the time kinetics and tissue distribution of CAM expression, the infiltration of mononuclear cells, and the expression of cytokines, identified by the in vitro studies as strong inducers or repressors of CAM in HSC, were analyzed. Wistar rats were provided by Charles River (Sulzfeld, Germany) and received humane care in compliance with the institution's guidelines and National Institutes of Health guidelines. To detect transcripts specific for CAM, polymerase chain reaction (PCR) generated cDNAs directed against rat N-CAM,12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar rat I-CAM-1, which mapped to positions 529–782 of the published sequence,13Kita Y Takashi T Iigo Y Tamatani T Miyasaka M Horiuchi T Sequence and expression of rat ICAM-1.Biochim Biophys Acta. 1992; 1131: 108-110Crossref PubMed Scopus (95) Google Scholar and against rat V-CAM-1, corresponding to positions 352–741 of the published sequence,14Williams AJ Atkins RC Fries JW Gimbrone MA Cybulsky MI Collins T Nucleotide sequence of rat vascular cell adhesion molecule-1 cDNA.Biochim Biophys Acta. 1992; 1131: 214-216Crossref PubMed Scopus (27) Google Scholar were used. Transforming growth factor (TGF)-β1-specific messengers were detected using a PCR-generated cDNA directed against rat TGF-β, which mapped to positions 763-1063 of the published sequence.15Qian SW Kondaiah P Roberts AB Sporn MB cDNA cloning by PCR of rat transforming growth factor-β1.Nucleic Acids Res. 1990; 18: 3059-3069Crossref PubMed Scopus (265) Google Scholar Furthermore, a PCR-generated cDNA directed against rat tumor necrosis factor (TNF)-α, which mapped to positions 140–509 of the published sequence,16Estler HC Grewe M Gaussling R Pavlovic M Decker K Rat tumor necrosis factor-α: transcription in rat Kupffer cells and in vitro posttranslational processing based on a PCR-derived cDNA.Biol Chem. 1992; 373: 271-281Google Scholar was used. In addition, clone pFH154 coding for human fibronectin17Kornblihtt A Vibe Pedersen K Baralle F Human fibronectin: molecular cloning evidence for two mRNA species differing by an internal segment coding for a structural domain.EMBO J. 1984; 3: 221-226Crossref PubMed Scopus (143) Google Scholar and a cDNA probe specific for human albumin18Kurnit DM Philipp BW Bruns GAP Confirmation of the mapping assignment of human serum albumin to chromosome 4 using a cloned human albumin gene.Cytogenet Cell Genet. 1982; 34: 282-288Crossref PubMed Scopus (24) Google Scholar were used. To validate quantitative Northern blot results a clone carrying the rat glycerylaldehyde-3-phosphod dehydropenase (GAPDH) cDNA19Fort P Marty L Piechaczyk M Sabrouty SE Dani C Jeanteur P Blanchard JM Various adult tissues express only one major mRNA species from the glyceraldehyde-3-phosphate-dehydrogenase multigenic family.Nucleic Acids Res. 1985; 13: 1431-1442Crossref PubMed Scopus (1972) Google Scholar or human β-actin20Ponte P Gunning P Blau H Kedes L Human actin genes are single copy for α-skeletal and α-cardiac actin but multicopy for β- and γ-cytoskeletal genes: 3′ untranslated regions are isotype specific but are conserved in evolution.Mol Cell Biol. 1983; 3: 1783-1791Crossref PubMed Google Scholar were used. Specificity of PCR products mentioned above was confirmed by digestion using appropriate restriction enzymes and by sequencing of cloned PCR products. PCR products were cloned using the TA cloning kit (Invitrogen, San Diego, CA) and sequenced using the Sequenase version 2.0 kit (United States Biochemical, Cleveland, OH). Sequence comparison was performed by Fasta or BestFit alignment programs of the genetics computer group package (Genetics Computer Group, Madison, WI) using standard parameters.21Devereux J Haeberli P Smithies O A comprehensive set of sequence analysis programs for the VAX.Nucleic Acids Res. 1984; 12: 387-395Crossref PubMed Scopus (11531) Google Scholar Monoclonal antibodies directed against rat I-CAM-1 were obtained from Genzyme (Cambridge, MA) and monoclonal antibodies directed against human V-CAM-1 (clone 51–10C9) from Pharmingen (San Diego, CA). A monoclonal anti N-CAM antibody (clone NCAM-OB11) was obtained from Sigma (Munich, Germany). The mAb against desmin, the antiserum directed against mouse IgGs, and the APAAP complex were from Dako (Copenhagen, Denmark). The mAbs directed against the ED1 and ED2 epitopes were from Biermann (Wiesbaden, Germany). The mAbs against smooth muscle alpha action (SMA) and antibodies directed against glial fibrillary acidic protein were from Sigma. The mAb against vimentin was from Boehringer (Mannheim, Germany) Cytokines were from the following sources and were tested at the concentrations provided below unless otherwise stated in the legends: TGF-β1, human, natural, 1 ng/ml (Sigma); insulin-like growth factor-1 (IGF-1), human, natural, 100 nMol (kindly provided by Dr. Märki, Ciba Geigy, Basel, Switzerland); platelet-derived growth factor (PDGF) (Sigma), human, natural, 10 ng/ml; epidermal growth factor (EGF), human, recombinant, 2.5 ng/ml (Sigma); hepatocyte growth factor (HGF), human, recombinant, 10 ng/ml (Sigma); TNF-α, human, recombinant, 100 U/ml (Genzyme); interferon-γ (IFN), rat, recombinant, 100 U/ml (Genzyme). HSC were isolated from rat liver and kept in primary culture as described previously.12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar, 22Knittel T Fellmer P Ramadori G Gene expression and regulation of plasminogen activator inhibitor type I in hepatic stellate cells of rat liver.Gastroenterology. 1996; 111: 745-754Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar, 23Knittel T Janneck T Müller L Fellmer P Ramadori G Transforming growth factor-β1 regulated gene expression of Ito cells.Hepatology. 1996; 24: 352-360Crossref PubMed Google Scholar, 24Knittel T Fellmer P Müller L Ramadori G Bone morphogenetic protein-6 is expressed in non parenchymal liver cells and upregulated by transforming growth factor-β1.Exp Cell Res. 1997; 232: 263-269Crossref PubMed Scopus (48) Google Scholar, 25Knittel T Fellmer P Neubauer K Kawakami M Grundmann A Ramadori G The complement activating protease P100 is expressed by hepatocytes and is induced by IL-6 in vitro und during the acute phase reaction in vivo.Lab Invest. 1997; 77: 221-230PubMed Google Scholar, 26Knittel T Müller L Saile B Ramadori G Effect of tumor necrosis factor-α on proliferation, activation and protein synthesis of rat hepatic stellate cells.J Hepatol. 1997; 27: 1067-1080Abstract Full Text PDF PubMed Scopus (70) Google Scholar As assessed by morphology and by the expression of SMA, GFAP, and N-CAM, HSC were considered fully activated at 7 days of primary culture and later, whereas cells cultured for 2 days were classified as resting HSC or HSC at an early stage of activation and cells cultured for 4 days were judged as transitional cells.12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar, 23Knittel T Janneck T Müller L Fellmer P Ramadori G Transforming growth factor-β1 regulated gene expression of Ito cells.Hepatology. 1996; 24: 352-360Crossref PubMed Google Scholar, 27Neubauer K Knittel T Aurisch S Fellmer P Ramadori G Glial fibrillary acidic protein: a cell type specific marker protein for Ito cells in vivo and in vitro.J Hepatol. 1996; 24: 719-730Abstract Full Text PDF PubMed Scopus (161) Google Scholar Purity of freshly isolated cells and cultured cells was assessed as stated earlier.12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar, 22Knittel T Fellmer P Ramadori G Gene expression and regulation of plasminogen activator inhibitor type I in hepatic stellate cells of rat liver.Gastroenterology. 1996; 111: 745-754Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar, 23Knittel T Janneck T Müller L Fellmer P Ramadori G Transforming growth factor-β1 regulated gene expression of Ito cells.Hepatology. 1996; 24: 352-360Crossref PubMed Google Scholar, 24Knittel T Fellmer P Müller L Ramadori G Bone morphogenetic protein-6 is expressed in non parenchymal liver cells and upregulated by transforming growth factor-β1.Exp Cell Res. 1997; 232: 263-269Crossref PubMed Scopus (48) Google Scholar, 25Knittel T Fellmer P Neubauer K Kawakami M Grundmann A Ramadori G The complement activating protease P100 is expressed by hepatocytes and is induced by IL-6 in vitro und during the acute phase reaction in vivo.Lab Invest. 1997; 77: 221-230PubMed Google Scholar, 26Knittel T Müller L Saile B Ramadori G Effect of tumor necrosis factor-α on proliferation, activation and protein synthesis of rat hepatic stellate cells.J Hepatol. 1997; 27: 1067-1080Abstract Full Text PDF PubMed Scopus (70) Google Scholar To verify that the CAM expression levels detected in HSC were not derived from other liver cells, hepatocytes, Kupffer cells, and sinusoidal endothelial cells were isolated from rat liver and cultivated as described previously.12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar, 22Knittel T Fellmer P Ramadori G Gene expression and regulation of plasminogen activator inhibitor type I in hepatic stellate cells of rat liver.Gastroenterology. 1996; 111: 745-754Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar, 24Knittel T Fellmer P Müller L Ramadori G Bone morphogenetic protein-6 is expressed in non parenchymal liver cells and upregulated by transforming growth factor-β1.Exp Cell Res. 1997; 232: 263-269Crossref PubMed Scopus (48) Google Scholar, 25Knittel T Fellmer P Neubauer K Kawakami M Grundmann A Ramadori G The complement activating protease P100 is expressed by hepatocytes and is induced by IL-6 in vitro und during the acute phase reaction in vivo.Lab Invest. 1997; 77: 221-230PubMed Google Scholar, 27Neubauer K Knittel T Aurisch S Fellmer P Ramadori G Glial fibrillary acidic protein: a cell type specific marker protein for Ito cells in vivo and in vitro.J Hepatol. 1996; 24: 719-730Abstract Full Text PDF PubMed Scopus (161) Google Scholar, 28Knittel T Armbrust T Neubauer K Ramadori G Expression of von Willebrand factor in normal and diseased rat livers and in cultivated liver cells.Hepatology. 1995; 21: 470-476PubMed Google Scholar, 29Neubauer K Eichorst S Wilfling T Buchenau M Xia L Ramadori G Sinusoidal intercellular adhesion molecule-1 up-regulation precedes the accumulation of leukocyte function antigen-1-positive cells and tissue necrosis in a model of carbontetrachloride-induced acute rat liver injury.Lab Invest. 1998; 78: 185-194PubMed Google Scholar HSC cultured for 2, 4, or 7 days were incubated for 20 hours in 1 ml serum reduced (0.3% fetal calf serum) culture medium with or without (controls) the mediators, which were used at the concentrations stated under “mediators.” Furthermore, the effects of increasing concentrations of TNF-α (1 U/ml, 10 U/ml, 100 U/ml and 1000 U/ml), TGF-β1 (0.1 ng/ml up to 10.0 ng/ml), or IGF-1 (1 nMol up to 100 nMol) were tested. At the end of the cytokine exposure, cells were processed for RNA extraction and Northern blot analysis as stated below. Experiments analyzing the regulation of CAM expression by mediators at the standard concentrations and 20-hour incubation periods testing HSC cultured for 2, 4, or 7 days were performed at least twice using at least two different HSC isolations. Rats were given carbon tetrachloride (CCl4)/maize oil solution (50%, v/v) orally as described earlier.12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar, 27Neubauer K Knittel T Aurisch S Fellmer P Ramadori G Glial fibrillary acidic protein: a cell type specific marker protein for Ito cells in vivo and in vitro.J Hepatol. 1996; 24: 719-730Abstract Full Text PDF PubMed Scopus (161) Google Scholar, 28Knittel T Armbrust T Neubauer K Ramadori G Expression of von Willebrand factor in normal and diseased rat livers and in cultivated liver cells.Hepatology. 1995; 21: 470-476PubMed Google Scholar Control animals were given maize oil only. Cryostat sections (5 μm) of normal or acutely damaged liver specimens and cells were fixed in methanol/acetone (5 minutes/10 seconds at −20°C) as described earlier.12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar, 27Neubauer K Knittel T Aurisch S Fellmer P Ramadori G Glial fibrillary acidic protein: a cell type specific marker protein for Ito cells in vivo and in vitro.J Hepatol. 1996; 24: 719-730Abstract Full Text PDF PubMed Scopus (161) Google Scholar, 28Knittel T Armbrust T Neubauer K Ramadori G Expression of von Willebrand factor in normal and diseased rat livers and in cultivated liver cells.Hepatology. 1995; 21: 470-476PubMed Google Scholar, 29Neubauer K Eichorst S Wilfling T Buchenau M Xia L Ramadori G Sinusoidal intercellular adhesion molecule-1 up-regulation precedes the accumulation of leukocyte function antigen-1-positive cells and tissue necrosis in a model of carbontetrachloride-induced acute rat liver injury.Lab Invest. 1998; 78: 185-194PubMed Google Scholar Cells or tissue sections were examined by the alkaline phosphatase anti-alkaline phosphatase (APAAP) staining procedure. Cells or tissue sections were incubated with specific primary antibodies for 1 hour at 37°C and were then covered for 1 hour at 37°C with an antiserum directed against mouse IgG followed by incubation with the APAAP complex. Nonspecific staining was controlled for by incubation with mouse Ig instead of the specific primary antibody. To compare the tissue distribution patterns of I-CAM-1, V-CAM-1, N-CAM, vimentin, desmin, GFAP, SMA, and ED1, serially cut tissue sections were prepared and analyzed. Cells were lysed with guanidinum isothiocyanate and total RNA was extracted as reported.12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar, 23Knittel T Janneck T Müller L Fellmer P Ramadori G Transforming growth factor-β1 regulated gene expression of Ito cells.Hepatology. 1996; 24: 352-360Crossref PubMed Google Scholar, 26Knittel T Müller L Saile B Ramadori G Effect of tumor necrosis factor-α on proliferation, activation and protein synthesis of rat hepatic stellate cells.J Hepatol. 1997; 27: 1067-1080Abstract Full Text PDF PubMed Scopus (70) Google Scholar For Northern blot analysis of the basal CAM expression levels, RNA prepared from four different cell preparations was pooled to overcome individual differences. The RNA (5 μg total) was resolved by agarose gel electrophoresis, transferred to nylon membranes, and hybridized with specific 32P-labeled cDNA probes. Hybridization was performed for 2 hours at 68°C using the QuickHyb Kit (Stratagene, La Jolla, CA). Posthybridization washes were performed 2 times for 15 minutes at room temperature and 1 time for 5–15 minutes at 60°C in 2× SSC containing 0.1% sodium dodecyl sulfate. Nylon filters were washed, dried, and exposed to x-ray films at −80°C. Using cDNAs generated by RT-PCR, I-CAM-1, V-CAM-1, and (as shown previously12Knittel T Aurisch S Neubauer K Eichhorst S Ramadori G Cell type specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver: up-regulation during in vitro activation and in hepatic tissue repair.Am J Pathol. 1996; 149: 449-462PubMed Google Scholar) N-CAM, coding transcripts were detected in HSC in vitro (Figure 1A). As reported for rat I-CAM-130Ban K Ikeda U Takahashi M Kanbe T Kasahara T Shimada K Expression of intercellular adhesion molecule-1 on rat cardiac myocytes by monocyte chemoattractant protein-1.Cardiovasc Res. 1994; 28: 1258-1262Crossref PubMed Scopus (50) Google Scholar and human or mouse V-CAM-1,31Rosenman S Shrikant P Dubb L Benveniste E Ransohoff R Cytokine-induced expression of vascular cell adhesion molecule-1 (VCAM-1) by astrocytes and astrocytoma cell lines.J Immunol. 1995; 154: 1888-1899PubMed Google Scholar, 32Fries JW Williams AJ Atkins RC Newman W Lipscomb MF Collins T Expression ov V-CAM-1 and E-selectin in an in vivo model of endothelial activation.Am J Pathol. 1993; 143: 725-737PubMed Google Scholar single I-CAM-1- and V-CAM-1-specific messengers of 3.0 kb and 3.2 kb in size were present in HSC from rat liver, respectively. Hybridization of filters containing RNA samples derived from hepatocytes, Kupffer cells, and sinusoidal endothelial cells of rat liver both directly after isolation and at different stages of primary culture indicated that the CAM expression of HSC was not derived from contaminating cells (data not shown).Figure 1Expression of cell adhesion molecules by HSC in vitro. A: Expression of I-CAM-1, V-CAM-1, and N-CAM as assessed by Northern blot analysis. Total RNA was purified from HSC at these time points: freshly isolated (0), day 2 or 3 (2/3), day 4 or 5 (4/5), day 7 (7), and day 9 or 10 (9/10) after plating. RNA (1.25 μg total) recovered from four different HSC isolations was pooled and size selected by 1% agaros" @default.
- W1500676217 created "2016-06-24" @default.
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- W1500676217 date "1999-01-01" @default.
- W1500676217 modified "2023-09-27" @default.
- W1500676217 title "Expression and Regulation of Cell Adhesion Molecules by Hepatic Stellate Cells (HSC) of Rat Liver" @default.
- W1500676217 cites W113046667 @default.
- W1500676217 cites W135460560 @default.
- W1500676217 cites W1514235737 @default.
- W1500676217 cites W1516756689 @default.
- W1500676217 cites W1536634718 @default.
- W1500676217 cites W15592170 @default.
- W1500676217 cites W1598333469 @default.
- W1500676217 cites W1600560134 @default.
- W1500676217 cites W1618952314 @default.
- W1500676217 cites W1686819669 @default.
- W1500676217 cites W169646064 @default.
- W1500676217 cites W1702287731 @default.
- W1500676217 cites W172343668 @default.
- W1500676217 cites W1769972265 @default.
- W1500676217 cites W1827819586 @default.
- W1500676217 cites W1909940207 @default.
- W1500676217 cites W1930570647 @default.
- W1500676217 cites W1964993697 @default.
- W1500676217 cites W1970938829 @default.
- W1500676217 cites W1974004289 @default.
- W1500676217 cites W1975439385 @default.
- W1500676217 cites W1975898748 @default.
- W1500676217 cites W1981871214 @default.
- W1500676217 cites W1985090011 @default.
- W1500676217 cites W1994614794 @default.
- W1500676217 cites W1996382554 @default.
- W1500676217 cites W1996765255 @default.
- W1500676217 cites W2000219166 @default.
- W1500676217 cites W2002327559 @default.
- W1500676217 cites W2004248423 @default.
- W1500676217 cites W2008380967 @default.
- W1500676217 cites W2008399598 @default.
- W1500676217 cites W2009049966 @default.
- W1500676217 cites W2009070596 @default.
- W1500676217 cites W2009310436 @default.
- W1500676217 cites W2011526233 @default.
- W1500676217 cites W2012641526 @default.
- W1500676217 cites W2013042426 @default.
- W1500676217 cites W2031094949 @default.
- W1500676217 cites W2031231091 @default.
- W1500676217 cites W2033805174 @default.
- W1500676217 cites W2040027819 @default.
- W1500676217 cites W2041613102 @default.
- W1500676217 cites W2042101513 @default.
- W1500676217 cites W2042288857 @default.
- W1500676217 cites W2042347883 @default.
- W1500676217 cites W2042626190 @default.
- W1500676217 cites W2045063455 @default.
- W1500676217 cites W2051819610 @default.
- W1500676217 cites W2055282796 @default.
- W1500676217 cites W2056463571 @default.
- W1500676217 cites W2062874643 @default.
- W1500676217 cites W2063495563 @default.
- W1500676217 cites W2077907876 @default.
- W1500676217 cites W2077969109 @default.
- W1500676217 cites W2079720530 @default.
- W1500676217 cites W2079812171 @default.
- W1500676217 cites W2082291632 @default.
- W1500676217 cites W2082645615 @default.
- W1500676217 cites W2084993681 @default.
- W1500676217 cites W2087100627 @default.
- W1500676217 cites W2088947646 @default.
- W1500676217 cites W2094354091 @default.
- W1500676217 cites W2117069079 @default.
- W1500676217 cites W2120525576 @default.
- W1500676217 cites W2122530058 @default.
- W1500676217 cites W2147819976 @default.
- W1500676217 cites W2167158568 @default.
- W1500676217 cites W228869535 @default.
- W1500676217 cites W2290154627 @default.
- W1500676217 cites W2327258270 @default.
- W1500676217 cites W2408757742 @default.
- W1500676217 cites W2417027714 @default.
- W1500676217 cites W2418174841 @default.
- W1500676217 cites W2465393583 @default.
- W1500676217 cites W2474068101 @default.
- W1500676217 cites W4231917310 @default.
- W1500676217 cites W4234463732 @default.
- W1500676217 cites W4238531876 @default.
- W1500676217 cites W4254527065 @default.
- W1500676217 cites W43608489 @default.
- W1500676217 cites W64951097 @default.
- W1500676217 doi "https://doi.org/10.1016/s0002-9440(10)65262-5" @default.
- W1500676217 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1853435" @default.
- W1500676217 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9916930" @default.
- W1500676217 hasPublicationYear "1999" @default.