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1.
Alcohol Clin Exp Res ; 25(5 Suppl ISBRA): 171S-181S, 2001 May.
Article in English | MEDLINE | ID: mdl-11391068

ABSTRACT

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Hidekazu Tsukamoto and Yoshiyuki Takei. The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated TNF signaling in alcoholic liver disease, by Craig J. McClain, S. Joshi-Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in ethanol-mediated sensitization of the liver, by Anna Colell, Carmen Garcia-Ruiz, Neil Kaplowitz, and Jose C. Fernandez-Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute ethanol administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S-adenosylmethionine affects tumor necrosis factor-alpha gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi-Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage TNFalpha gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut-derived endotoxin in alcoholic liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.


Subject(s)
Gene Expression/physiology , Liver Diseases, Alcoholic/etiology , Liver/drug effects , Mitochondria, Liver/drug effects , Superoxides/metabolism , Tumor Necrosis Factor-alpha/metabolism , Animals , Bezafibrate/pharmacology , Endotoxins/metabolism , Gene Expression/drug effects , Hepatocytes/drug effects , Hepatocytes/metabolism , Humans , Hypolipidemic Agents/pharmacology , Iron/metabolism , Kupffer Cells/drug effects , Kupffer Cells/metabolism , Liver/metabolism , Liver Diseases, Alcoholic/metabolism , Mitochondria, Liver/metabolism , Peroxisome Proliferators/pharmacology , S-Adenosylmethionine/metabolism , Tretinoin/metabolism
2.
Alcohol Clin Exp Res ; 25(5 Suppl ISBRA): 182S-188S, 2001 May.
Article in English | MEDLINE | ID: mdl-11391069

ABSTRACT

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Toshio Narahashi and Kinya Kuriyama. The presentations were (1) Modulation of neuroreceptors and ion channels by alcohol, by T. Narahashi; (2) Inhibition by ethanol of NMDA and AMPA receptor-channels, by P. Illes, K. Wirkner, W. Fischer, K. Mühlberg, P. Scheibler, and C. Allgaier; (3) Effects of ethanol on metabotropic glutamate receptors, by K. Minami; (4) Acute alcohol actions on the 5-HT3 ligand-gated ion channel, by D. Lovinger; (5) Inhibition of NMDA receptors by MK801 attenuates ethanol-induced taurine release from the hippocampus, by F. Lallemand, R.J. Ward, and P. DeWitte; and (6) Effect of ethanol on voltage-operated Ca2+ channels in hepatic stellate cells, by T. Itatsu, Y. Takei, H. Oide, M. Hirose, X. E. Wang, S. Watanabe, M. Tateyama, R. Ochi, and N. Sato.


Subject(s)
Calcium Channels/drug effects , Central Nervous System Depressants/pharmacology , Ethanol/pharmacology , Receptors, AMPA/drug effects , Receptors, Metabotropic Glutamate/drug effects , Receptors, N-Methyl-D-Aspartate/drug effects , Animals , Calcium Channels/physiology , Hippocampus/drug effects , Hippocampus/physiology , Humans , Ion Channels/drug effects , Ion Channels/physiology , Receptors, AMPA/physiology , Receptors, Metabotropic Glutamate/physiology , Receptors, N-Methyl-D-Aspartate/physiology , Receptors, Serotonin/drug effects , Receptors, Serotonin/physiology , Receptors, Serotonin, 5-HT3 , Sensory Receptor Cells/drug effects , Sensory Receptor Cells/metabolism
3.
Alcohol Clin Exp Res ; 24(4 Suppl): 55S-58S, 2000 Apr.
Article in English | MEDLINE | ID: mdl-10803781

ABSTRACT

BACKGROUND: Ethanol causes both tolerance and sensitization of Kupffer cells. Accordingly, this study examines the effect of acute ethanol consumption on nitric oxide (NO) production from Kupffer cells with or without lipopolysaccharide (LPS) treatment. METHODS: Rats were given ethanol (4 g/kg body weight) intragastrically, and Kupffer cells were isolated 2 and 24 hr later. Some rats were treated for 4 days with 150 mg/kg/day of polymyxin B and 450 mg/kg/day of neomycin to prevent growth of intestinal bacteria, the primary source of endotoxin in the gastrointestinal tract. After addition of LPS, NO was measured by the Griess reaction. RESULTS: Two hours after ethanol administration, LPS-induced NO production by Kupffer cells was diminished by 50% but was enhanced 2-fold at 24 hr. Sterilization of the gut with antibiotics blocked this enhancement. CONCLUSIONS: Kupffer cells isolated from rats early after ethanol exhibited tolerance to LPS, whereas sensitization was observed later. It is likely that sensitization to Kupffer cell is caused by gut-derived endotoxin.


Subject(s)
Ethanol/pharmacology , Kupffer Cells/drug effects , Kupffer Cells/metabolism , Lipopolysaccharides/pharmacology , Nitric Oxide/biosynthesis , Animals , Anti-Bacterial Agents/pharmacology , Drug Interactions , Female , Kinetics , Rats , Rats, Sprague-Dawley
4.
Aliment Pharmacol Ther ; 14 Suppl 1: 176-82, 2000 Apr.
Article in English | MEDLINE | ID: mdl-10807421

ABSTRACT

BACKGROUND: Aspirin is known to cause adverse effects, including gastric mucosal injury, and to retard gastric wound healing. Growth factors including hepatocyte growth factor (HGF), epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I) have been shown to play an important role in the repair of gastric mucosal injury. AIM: To employ the cultured gastric epithelial cell model to elucidate the effects of aspirin, as well as several growth factors (HGF, EGF and IGF-I), on gastric wound repair. METHODS: Isolated rabbit gastric epithelial cells (92% mucous cells) were cultured in F-12 medium and formed a complete monolayer cell sheet in 48 h. A wound with a cell-free area of constant size (2 mm2) was then created and the wound repair process was monitored by measuring wound size every 12 h. Proliferating cells were detected by BrdU staining. Effects of aspirin (8 mM), HGF (10 ng/mL), EGF (10 ng/mL) and IGF-I (30 ng/mL) were assessed. RESULTS: Aspirin significantly retarded wound healing, but simultaneous addition of growth factors significantly accelerated wound repair compared with aspirin alone. Growth factors reversed the aspirin-induced inhibition of cell proliferation. CONCLUSION: Growth factors, including HGF, EGF and IGF-I, reversed the aspirin-induced inhibition of wound repair through their cytoprotective effects on gastric epithelial cells.


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Aspirin/adverse effects , Epidermal Growth Factor/pharmacology , Epithelial Cells/physiology , Gastric Mucosa/pathology , Hepatocyte Growth Factor/pharmacology , Insulin-Like Growth Factor I/pharmacology , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Aspirin/pharmacology , Cell Culture Techniques , Cell Division/drug effects , Cytoprotection , Rabbits
6.
J Gastroenterol Hepatol ; 15 Suppl: D20-5, 2000 Mar.
Article in English | MEDLINE | ID: mdl-10759216

ABSTRACT

The hepatotoxic effects of alcohol have been described in detail, but factors responsible for its hepatotoxicity have only partially been characterized. For example, it is known that chronic ethanol ingestion increases hepatotoxicity and produces fatty liver, hepatitis and cirrhosis. However, acute ethanol consumption reduces endotoxin hepatotoxicity. It now appears that Kupffer cells participate in several aspects of these phenomena. Previously, most studies on the effects of alcohol on liver function have focused chiefly on the hepatocyte. Recently, attention has been directed towards the effect of ethanol ingestion on Kupffer cell function, which is stimulated by gut-derived endotoxins (lipopolysaccharides) via mechanisms dependent on increased gut permeability and the possible relationship between Kupffer cells and alcohol-induced liver injury. Here we will review new evidence for the proposal that Kupffer cells and endotoxins play a pivotal role in hepatotoxicity following alcohol exposure, based on studies using the continuous intragastric enteral feeding model developed by Tsukamoto and French and an acute model developed by us.


Subject(s)
Kupffer Cells/physiology , Lipopolysaccharides/metabolism , Liver Diseases, Alcoholic/etiology , Ethanol/pharmacology , Female , Humans , Male , Sex Factors
7.
Alcohol Clin Exp Res ; 24(3): 357-60, 2000 Mar.
Article in English | MEDLINE | ID: mdl-10776676

ABSTRACT

BACKGROUND: Hepatic stellate cells have been reported to play important roles in the regulation of hepatic microcirculation via cell contraction. Increase in intracellular calcium concentration is required to induce cell contraction. We have already reported the existence of L-type voltage-operated Ca2+ channels (VOCC), such as smooth muscle cells. On the other hand, alcohol has been known to disturb hepatic microcirculation. In this study, we evaluated the effect of acute and chronic treatment of alcohol on VOCC in rat hepatic stellate cells. METHODS: Stellate cells isolated from rats were cultured with or without 100 mM ethanol for up to 14 days. VOCC were detected by the patch clamp technique. Cells cultured for 14 days without ethanol were exposed to ethanol to investigate calcium current during membrane depolarization. alpha-Smooth muscle actin (alpha-SMA) was stained by indirect immunofluorescence. RESULTS: In the control model, VOCC were recognized in cells cultured for more than 7 days. Detection of VOCC increased from 9% on day 7 to 55% on day 14. On the other hand, VOCC in cells treated chronically with 100 mM ethanol appeared earlier than in the control and the incidences were significantly higher than those of the control accompanied with an early activation of cells. In contrast, simultaneous exposure to ethanol during the membrane depolarization inhibited Ca2+ current. CONCLUSIONS: The expression of Ca2+ channels in stellate cells were up-regulated by the chronic treatment of alcohol accompanied with the transformation to myofibroblast-like phenotype. However, alcohol itself inhibited Ca2+ current.


Subject(s)
Calcium Channels/drug effects , Central Nervous System Depressants/pharmacology , Ethanol/pharmacology , Liver/drug effects , Actins/drug effects , Actins/metabolism , Animals , Calcium Channels/physiology , Cells, Cultured , Endothelium/cytology , Female , Liver/cytology , Liver/physiology , Rats , Rats, Wistar
9.
Biochim Biophys Acta ; 1418(1): 158-64, 1999 Apr 14.
Article in English | MEDLINE | ID: mdl-10209220

ABSTRACT

We previously reported stellate (Ito) cells possess voltage-activated Ca2+ current. The activation of stellate cells has been indicated to contribute to liver fibrosis and the regulation of hepatic hemodynamics. The aim of this study was to investigate the relationship between voltage-activated Ca2+ current and activation of stellate cells. Voltage-activated Ca2+ current in stellate cells isolated from rats were studied using whole-cell patch clamp technique. L-type voltage-activated Ca2+ current was hardly detected in stellate cells cultured for less than 9 days. Ca2+ current was detected 12.5 and 69% of cells at the 10th and 14th day of culture, respectively. BrdU incorporation indicated cell proliferation was recognized over 50% of cells at the 3rd and 5th day of culture, respectively, then decreased significantly in a time-dependent manner. On the other hand, the expression of alpha-smooth muscle actin indicated cell activation increased from 7th day of culture and collagen type I mRNA appeared remarkably in cells cultured for more than 10 days. In this study, we concluded L-type voltage-activated Ca2+ current was recognized in activated stellate (myofibroblast-like) cells.


Subject(s)
Calcium Channels/metabolism , Liver/metabolism , Muscle, Smooth/metabolism , Actins/analysis , Animals , Blotting, Western , Cell Division , Cells, Cultured , Collagen/genetics , Desmin/analysis , Female , Patch-Clamp Techniques , RNA, Messenger/analysis , Rats , Rats, Sprague-Dawley , Reverse Transcriptase Polymerase Chain Reaction
11.
Aliment Pharmacol Ther ; 12(11): 1131-8, 1998 Nov.
Article in English | MEDLINE | ID: mdl-9845403

ABSTRACT

BACKGROUND: Although the detailed mechanism is unclear, zinc and its derivative, polaprezinc, have been reported to accelerate gastric ulcer healing in vivo. AIM: To investigate the detailed cellular mechanism of polaprezinc on gastric epithelial cells and fibroblasts with special attention to insulin-like growth factor I (IGF-I). METHODS: Isolated rabbit gastric epithelial cells formed a complete monolayer, from which a circular artificial wound with constant size was made. The restoration process was monitored by measuring wound size up to 48 h. Either polaprezinc, IGF-I, fibroblast conditioned medium or neutralized medium conditioned by anti-IGF-I antibody was added at the time of wounding. The expression of mRNA of IGF-I, hepatocyte growth factor (HGF) and transforming growth factor alpha (TGF-alpha) in fibroblasts with or without polaprezinc treatment was tested using reverse transcription polymerase chain reaction (RT-PCR). Gastric epithelial cell proliferation was also examined by bromodeoxyuridine (BrdU) staining. RESULTS: IGF-I and fibroblast conditioned medium treatment accelerated gastric epithelial restoration which included cell migration and proliferation. However, polaprezinc and neutralized conditioned medium treatment did not accelerate epithelial repair. RT-PCR for growth factor mRNA revealed the IGF-I mRNA expression in fibroblasts was increased after treatment with polaprezinc. CONCLUSION: Polaprezinc induced IGF-I production from mesenchymal cells, resulting in stimulation of epithelial cell restoration through a paracrine pathway. IGF-I may play an important role in gastric wound repair.


Subject(s)
Carnosine/analogs & derivatives , Gastric Mucosa/drug effects , Insulin-Like Growth Factor I/pharmacology , Organometallic Compounds/pharmacology , Wound Healing/drug effects , Animals , Blotting, Southern , Carnosine/pharmacology , Cell Division/drug effects , Cell Movement/drug effects , Cells, Cultured , Fibroblasts/metabolism , Gastric Mucosa/cytology , Gene Expression , Growth Substances/analysis , Insulin-Like Growth Factor I/genetics , Male , Mesoderm , RNA, Messenger/metabolism , Rabbits , Reverse Transcriptase Polymerase Chain Reaction , Zinc Compounds
12.
Biochem Biophys Res Commun ; 251(2): 533-7, 1998 Oct 20.
Article in English | MEDLINE | ID: mdl-9792808

ABSTRACT

Hepatic stellate cells (HSCs) have L-type voltage-operated Ca2+ channels (VOCC). However, the effect of ethanol on VOCC is unknown. To investigate the mechanism of ethanol-induced liver injury, the effect of ethanol on VOCC in HSCs was studied. In control cells, VOCC revealed by patch clamp techniques were not detected in cells cultured for less than 7 days; however, a faint VOCC mRNA by reverse-transcription polymerase chain reaction was recognized at the 5(th) day of culture. Detection of VOCC increased from 8% on day 7 to over 50% on day 14 in controls. With ethanol (100mM), it increased from 12% on day 5 to 100 % on day 14. Furthermore, expression of alpha-smooth muscle actin, shown as transformation to a myofibroblast, was recognized in ethanol-treated cells earlier and stronger than that in controls. VOCC were up-regulated by the treatment with ethanol associated with the induction of transformation to myofibroblasts.


Subject(s)
Calcium Channels/genetics , Ethanol/pharmacology , Gene Expression Regulation/drug effects , Liver/metabolism , Transcription, Genetic , Actins/genetics , Animals , Calcium/metabolism , Calcium Channels/physiology , Calcium Channels, L-Type , Cell Differentiation/drug effects , Cells, Cultured , Female , Fibroblasts/cytology , Kinetics , Liver/cytology , Liver/drug effects , Patch-Clamp Techniques , RNA, Messenger/biosynthesis , Rats , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Time Factors , Transcription, Genetic/drug effects
13.
J Gastroenterol Hepatol ; 13 Suppl: S14-8, 1998 Sep.
Article in English | MEDLINE | ID: mdl-9792030

ABSTRACT

Prostaglandin E1 (PGE1) has been reported to have, experimentally and clinically, a protective effect against liver damage. This effect may result from the relaxation of hepatic stellate cells, whose contraction induces vasoconstriction of hepatic sinusoids. However, prostaglandins are unstable and a new drug delivery system is necessary to administer a sufficient amount of prostaglandin to achieve a protective effect in the liver. The aim of the study is to investigate the effects of lipo-prostaglandin E1 (lipo-PGE1) which has a novel drug delivery system on the stellate cell contraction induced by endothelin-1 in vitro. Lipo-PGE1 inhibited endothelin-1-induced stellate cell contraction in concentrations of 10, 30 and 50 ng/mL. Therefore, lipo-PGE1 may show a cytoprotective effect in the liver through the relaxation of stellate cells and an increase in the hepatic sinusoidal blood flow.


Subject(s)
Alprostadil/pharmacology , Liver/cytology , Alprostadil/metabolism , Animals , Cells, Cultured , Endothelin-1/pharmacology , Male , Rats , Rats, Wistar
14.
Biochem Biophys Res Commun ; 250(2): 486-90, 1998 Sep 18.
Article in English | MEDLINE | ID: mdl-9753658

ABSTRACT

Limited data exist regarding morphogenesis and differentiation during liver regeneration. We examined the role of epimorphin on liver regeneration. After 70% partial hepatectomy, mouse liver was collected on days 1, 3, 7, and 14 for immunohistochemistry and the detection of epimorphin mRNA and connexin 32. Using primary cultured rat hepatocytes, morphogenesis and differentiation of cells were tested with or without epimorphin. Seven days after cell inoculation, the expression of connexin 32 and the cell-cell communication was tested as a marker of differentiation. Epimorphin was detected exclusively in hepatic stellate cells. Connexin 32 was detected only in hepatocytes. After partial hepatectomy, epimorphin mRNA was detected on day 3 and peaked at day 7, followed by protein expression. Connexin 32 expression showed a similar time course. Cultured hepatocytes formed multicellular spheroids in an active epimorphin-coated culture dish and showed positive dye coupling, whereas the cell-cell communication was lost without active epimorphin. Because epimorphin was expressed late in liver regeneration, it might play a role in morphogenesis and differentiation.


Subject(s)
Connexins/physiology , Liver Regeneration , Membrane Glycoproteins/physiology , Animals , Cell Communication/physiology , Mice , Mice, Inbred BALB C , Rats , Rats, Wistar , Gap Junction beta-1 Protein
15.
Article in Japanese | MEDLINE | ID: mdl-9701995

ABSTRACT

The purpose of this study was to clarify the effect of ethanol on restoration of gastric epithelial cells after artificial cell-free area was made in the culture dish. Restoration of such "wounding" was evaluated quantitatively every 12 hr using a computer image analyzer with and without ethanol. Without ethanol, restoration was achieved within 48 hr. Exposure to ethanol retarded cellular restoration significantly. BrdU-positive cells were recognized around the wound from 24 to 36 hr, and then decreased substantially in control. However, BrdU-positive cells were rarely detected in ethanol group. Staining for actin in the control group revealed the presence of lamellipodia and stress fibers. However, the ethanol groups were observed in narrowed lamellipodia and few stress fibers. In conclusion, ethanol retarded the migration and proliferation of cultured gastric mucosal cells after in vitro wounding, possibly by damaging the cytoskeletal system. To evaluate cell mature during restoration of gastric mucosa after ethanol ingestion, the expression of gap junction protein connexin 32 was studied. The injury was most severe 1h after treatment, and was completely resolved by the 4th day after treatment. The number of immunoreactive spots for gap junctions was markedly decreased 1h after treatment. Reappearance of these staining occurred with repair of the injury. The reappearance of connexin 32 was delayed in comparison with both the histological resolution of the injury and the normalization of PAS-stained mucus. The most active cell proliferation stained by BrdU was observed 24h and then normalized 14th day after treatment. These results indicate that morphological repair is different to the recovery of cell maturity and cell proliferation in the regenerative gastric mucosa.


Subject(s)
Ethanol/adverse effects , Gastric Mucosa/physiology , Regeneration/drug effects , Actins/metabolism , Animals , Bromodeoxyuridine/metabolism , Cell Division/drug effects , Cells, Cultured , Depression, Chemical , Gastric Mucosa/cytology , Gastric Mucosa/drug effects , Humans , Male , Rabbits , Rats , Rats, Wistar
16.
J Gastroenterol ; 33(2): 153-9, 1998 Apr.
Article in English | MEDLINE | ID: mdl-9605942

ABSTRACT

The mechanism of action of gastrocytoprotective agents is not fully understood. We assessed the effects of an anti-ulcer agent, teprenone, and bile acid on epithelial restoration. Teprenone with or without deoxycholic acid was added to a complete confluent cultured gastric epithelial cell sheet after wounding. Restoration was monitored for 48 h, and the wound size was assessed. Migration velocity was measured, and proliferation was detected by sequential staining with bromodeoxyuridine. The labeling index was calculated. Restoration was completed within 48h in controls, whereas deoxycholic acid retarded repair. The migration velocity was suppressed by deoxycholic acid treatment. The number of proliferative cells peaked at 36 h (labeling index, 1.7%) in controls. In the deoxycholic acid group, the maximal labeling index was 0.5% at 48 h. Teprenone abolished the bile acid-induced retardation. Teprenone showed cytoprotective effects against deoxycholic acid-induced inhibition of epithelial cell migration and proliferation.


Subject(s)
Anti-Ulcer Agents/pharmacology , Diterpenes/pharmacology , Gastric Mucosa/cytology , Animals , Bile Acids and Salts/pharmacology , Cell Movement/drug effects , Cells, Cultured , Cytoprotection , Deoxycholic Acid/pharmacology , Epithelial Cells/drug effects , Gastric Mucosa/drug effects , Male , Rabbits
18.
Aliment Pharmacol Ther ; 10(6): 927-32, 1996 Dec.
Article in English | MEDLINE | ID: mdl-8971290

ABSTRACT

BACKGROUND: Anti-ulcer agents exert various functional effects on gastric epithelial cells. AIM: The effects of a novel gastro-cytoprotective agent (rebamipide) on epithelial restoration following bile acid damage were assessed using primary cultured rabbit gastric epithelial cells. METHODS: Rebamipide was added to complete confluent cell sheets with deoxycholic acid just after creating a cell-free wound (2 mm2). The restoration was monitored and analysed by phase contrast microscopy and an image analyser for 48 h. The migration speed was measured during the initial 3 h after wounding. Cell proliferation was detected by staining for bromodeoxyuridine (BrdU) at 12-h intervals. The labelling index was calculated per unit area. The major cytoskeletal protein actin was detected by immunohistochemical staining. RESULTS: In the controls, restoration was completed 48 h following wounding. Deoxycholic acid retarded this process. The addition of rebamipide to deoxycholic acid abolished the bile acid-induced retardation. The migration speed was 26 microns/h in the controls. 15 microns/h in the deoxycholic acid group and 27 microns/h in the deoxycholic acid plus rebamipide group. In the controls, BrdU-positive cells, which were rarely detected in the initial 24 h, were maximal at 36 h (labelling index 1.7%). In the deoxycholic acid group, proliferation was inhibited (peak labeling index; 0.5% at 48 h). Actin-containing stress fibres were detected throughout the cells and the periphery of the lamellipodia in the controls, and were disrupted in the deoxycholic acid-treated group. Rebamipide prevented these effects. CONCLUSIONS: Deoxycholic acid significantly retarded restoration by the inhibition of both cell migration and proliferation, potentially through an effect on the cytoskeleton. Rebamipide protected the mucosal cells from bile acid mediated injury.


Subject(s)
Alanine/analogs & derivatives , Anti-Ulcer Agents/pharmacology , Gastric Mucosa/cytology , Gastric Mucosa/drug effects , Quinolones/pharmacology , Stomach Diseases/drug therapy , Actins/analysis , Alanine/pharmacology , Animals , Bromodeoxyuridine/metabolism , Cell Division/drug effects , Cell Movement/drug effects , Cells, Cultured , Deoxycholic Acid/toxicity , Disease Models, Animal , Epithelial Cells , Epithelium/drug effects , Epithelium/metabolism , Gastric Mucosa/metabolism , Male , Rabbits , Staining and Labeling/methods , Stomach Diseases/chemically induced , Stomach Diseases/pathology
19.
Biochem Biophys Res Commun ; 225(1): 155-60, 1996 Aug 05.
Article in English | MEDLINE | ID: mdl-8769110

ABSTRACT

A novel mesenchymal protein, epimorphin, has been reported to play a key role in morphogenesis of fetal organs. The morphological and functional features of epimorphin in adult liver were entirely unknown. This study was performed to determine the distribution and function of this protein in the adult mouse liver. Epimorphin was detected on sinusoidal Ito cells. It played an essential role in the formation of hepatocyte spheroids which maintained differentiated function in primary culture. Therefore, Ito cells might control the differentiation of parenchymal hepatocytes in the adult liver in the pathologic condition as well as in fetal organs.


Subject(s)
Liver/cytology , Membrane Glycoproteins/physiology , Animals , Bile Canaliculi/cytology , Bile Canaliculi/ultrastructure , Cells, Cultured , Desmin/analysis , Fluorescent Antibody Technique , Immunohistochemistry , Liver/physiology , Male , Mice , Mice, Inbred BALB C , Microscopy, Electron , Morphogenesis , Serum Albumin/metabolism
20.
Scand J Gastroenterol ; 31(4): 391-7, 1996 Apr.
Article in English | MEDLINE | ID: mdl-8726309

ABSTRACT

BACKGROUND: The cytoskeletal system is believed to play an important role in normal bile formation. The effects of wortmannin, a new myosin light-chain kinase inhibitor, on bile canalicular contraction and bile flow have been observed. METHODS: The bile canalicular contraction of cultured hepatocyte doublets was investigated, using an image analyzer with a phase contrast microscope, and the intracellular Ca2+ concentration was measured, using microscopic fluorometry. We also investigated bile flow by in vivo intraportal infusion of the drug in rats. RESULTS: Treatment with wortmannin inhibited norepinephrine-induced canalicular contraction and caused a decrease in bile flow without changing systematic and portal blood pressure. Morphologic examination of the electron microscopic study showed that most bile canaliculi were dilated, with loss of microvilli, but no other apparent damage was seen in parenchymal hepatocytes. CONCLUSIONS: These data suggest that the integrity of the phosphorylation system of myosin is essential for normal bile flow.


Subject(s)
Androstadienes/pharmacology , Bile Canaliculi/drug effects , Myosin-Light-Chain Kinase/antagonists & inhibitors , Animals , Bile/physiology , Bile Canaliculi/physiology , Calcium/analysis , Cells, Cultured , Female , In Vitro Techniques , Liver/drug effects , Microscopy, Electron , Microscopy, Phase-Contrast , Myosins/physiology , Rats , Rats, Wistar , Wortmannin
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