Structural modifications of intercellular junctions.

1978 ◽  
Vol 36 (2) ◽  
pp. 330-331
Author(s):  
J. Metz ◽  
M. Merlo ◽  
W. G. Forssmann
Keyword(s):  
Gap Junctions ◽  
Intercellular Junctions ◽  
Cell Isolation ◽  
Extrahepatic Cholestasis ◽  
Structural Modifications ◽  
Pancreatic Duct Ligation ◽  
Pancreatic Cells ◽  
Duct Ligation ◽  
Thin Sectioning ◽  
And Function

Structure and function of intercellular junctions were studied under the electronmicroscope using conventional thin sectioning and freeze-etch replicas. Alterations of tight and gap junctions were analyzed 1. of exocrine pancreatic cells under cell isolation conditions and pancreatic duct ligation and 2. of hepatocytes during extrahepatic cholestasis.During the different steps of cell isolation of exocrine pancreatic cells, gradual changes of tight and gap junctions were observed. Tight junctions, which formed belt-like structures around the apex of control acinar cells in situ, subsequently diminished, became interrupted and were concentrated into macular areas (Fig. 1). Aggregations of membrane associated particles, which looked similar to gap junctions, were intermixed within tight junctional areas (Fig. 1). These structures continously disappeared in the last stages of the isolation procedure. The intercellular junctions were finally separated without destroying the integrity of the cell membrane, which was confirmed with porcion yellow, lanthanum chloride and horse radish peroxidase.

scholarly journals Mechanisms of Biliary Damage

2010 ◽  
Vol 3 ◽  
pp. JCD.S2785 ◽  
Author(s):  
Fuquan Yang ◽  
Eugenio Gaudio ◽  
Paolo Onori ◽  
Candace Wise ◽  
Gianfranco Alpini ◽  
...  
Keyword(s):  
Cell Death ◽  
Bile Duct ◽  
In Vitro Models ◽  
Experimental Models ◽  
Treatment Modalities ◽  
Extrahepatic Cholestasis ◽  
Therapeutic Modalities ◽  
Duct Ligation ◽  
And Function

Bile duct damage is present in virtually all cholangiopathies, which share the biliary epithelial cells (i.e. cholangiocytes) as a common pathogenic target. Cholangiocyte cell death largely occurs through the process of apoptosis. In this review, we will summarize the mechanisms through which biliary damage occurs in a variety of animal and in vitro models, such as extrahepatic cholestasis induced by bile duct ligation (BDL), cytotoxin- and hepatotoxin-induced liver injury, and biliary atresia. Although we have increased our knowledge of the factors that regulate cholangiocyte cell death mechanisms during cholangiopathies, especially in experimental models, there is still a lack of effective treatment modalities for these biliary disorders. However, future studies will hopefully provide for new therapeutic modalities for the prevention or restoration of biliary mass and function lost during the progression of cholangiopathies.

Quantitative EM of gap junction distribution in mutant drosophila wing discs

1983 ◽  
Vol 41 ◽  
pp. 720-721
Author(s):  
J.S. Ryerse
Keyword(s):  
Gap Junctions ◽  
Growth Control ◽  
Intercellular Junctions ◽  
Wing Disc ◽  
En Bloc ◽  
Metabolic Cooperation ◽  
Drosophila Wing ◽  
Adult Wing ◽  
Wing Discs ◽  
Wing Pouch

Gap junctions are intercellular junctions found in both vertebrates and invertebrates through which ions and small molecules can pass. Their distribution in tissues could be of critical importance for ionic coupling or metabolic cooperation between cells or for regulating the intracellular movement of growth control and pattern formation factors. Studies of the distribution of gap junctions in mutants which develop abnormally may shed light upon their role in normal development. I report here the distribution of gap junctions in the wing pouch of 3 Drosophila wing disc mutants, vg (vestigial) a cell death mutant, 1(2)gd (lethal giant disc) a pattern abnormality mutant and 1(2)gl (lethal giant larva) a neoplastic mutant and compare these with wildtype wing discs.The wing pouch (the anlagen of the adult wing blade) of a wild-type wing disc is shown in Fig. 1 and consists of columnar cells (Fig. 5) joined by gap junctions (Fig. 6). 14000x EMs of conventionally processed, UA en bloc stained, longitudinally sectioned wing pouches were enlarged to 45000x with a projector and tracings were made on which the lateral plasma membrane (LPM) and gap junctions were marked.

scholarly journals Publisher Correction: Pancreatic duct ligation reduces premalignant pancreatic lesions in a Kras model of pancreatic adenocarcinoma in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Marta Cáceres ◽  
Rita Quesada ◽  
Mar Iglesias ◽  
Francisco X. Real ◽  
Maria Villamonte ◽  
...  
Keyword(s):  
Pancreatic Duct ◽  
Pancreatic Adenocarcinoma ◽  
Pancreatic Duct Ligation ◽  
Duct Ligation

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

scholarly journals Topology and quaternary structure of pro-sucrase/isomaltase and final-form sucrase/isomaltase

1986 ◽  
Vol 237 (2) ◽  
pp. 455-461 ◽  
Author(s):  
G M Cowell ◽  
J Tranum-Jensen ◽  
H Sjöström ◽  
O Norén
Keyword(s):  
Electron Microscopy ◽  
Quaternary Structure ◽  
Functional Organization ◽  
Enzyme Complex ◽  
Single Chain ◽  
Pancreatic Duct Ligation ◽  
Duct Ligation ◽  
Catalytically Active ◽  
Identical Series ◽  
Dimeric Model

Pig sucrase/isomaltase (EC 3.2.1.48/10) was purified from intestinal microvillar vesicles prepared from animals with and without pancreatic-duct ligation to obtain the single-chain pro form and the proteolytically cleaved final form respectively. The purified enzymes were re-incorporated into phosphatidylcholine vesicles and analysed by electron microscopy after negative staining. The two forms of the enzyme were observed as identical series of characteristic projected views that could be unified in a single dimeric model, containing two sucrase and two isomaltase units. This shows a homodimeric functional organization similar to that of other microvillar hydrolases. The bulk of the dimer was separated from the membrane by a maximal gap of 3.5 nm, representing a junctional segment connecting the intramembrane section of the anchor to the catalytically active domain of sucrase/isomaltase. The enzyme complex protrudes from the membrane for a distance of up to 17 nm. From charge-shift immunoelectrophoresic studies of hydrophilic prosucrase/isomaltase and from electron microscopy of reconstituted pro-sucrase/isomaltase, there was no evidence to suggest the presence of anchoring sequences between the sucrase and isomaltase subunits.

scholarly journals Somatostatin levels and binding in duodenal mucosa of rabbits with ligation of the pancreatic duct

1988 ◽  
Vol 118 (2) ◽  
pp. 227-232 ◽  
Author(s):  
L. G. Guijarro ◽  
E. Arilla
Keyword(s):  
Pancreatic Duct ◽  
Binding Sites ◽  
Exocrine Pancreas ◽  
Duodenal Mucosa ◽  
Physiological Significance ◽  
Scatchard Analysis ◽  
Pancreatic Duct Ligation ◽  
Parallel Increase ◽  
Duct Ligation ◽  
Number Of Binding Sites

ABSTRACT Atrophy of the exocrine pancreas was induced in rabbits by pancreatic duct ligation. Somatostatin concentration and binding in cytosol from rabbit duodenal mucosa were studied after 6 and 14 weeks of pancreatic duct ligation. Somatostatin-like immunoreactivity was significantly increased in the duodenal mucosa in both periods. Scatchard analysis showed a parallel increase in the number of binding sites rather than a change in their affinity. The physiological significance of these findings remains to be clarified. J. Endocr. (1988) 118, 227–232

Are gap junctions necessary for cell-to-cell coupling of smooth muscle?: an update

1992 ◽  
Vol 70 (4) ◽  
pp. 481-490 ◽  
Author(s):  
R. E. Garfield ◽  
G. Thilander ◽  
M. G. Blennerhassett ◽  
N. Sakai
Keyword(s):  
Smooth Muscle ◽  
Gap Junctions ◽  
Current Knowledge ◽  
Smooth Muscles ◽  
Cell Communication ◽  
Circular Muscle ◽  
Cell Coupling ◽  
And Function ◽  
Longitudinal Layer ◽  
Cell Cell

Earlier, it was questioned whether gap junctions (GJs) were necessary for cell–cell communication in smooth muscle, and GJs were not seen in some smooth muscles. We reexamined this question in the myometrium and in intestinal smooth muscle, in light of current knowledge of the presence and function of GJs. In the uterus, numerous studies show that an increase in GJ number is associated with the onset of delivery and is required for effective parturition. In all cases, this increase in GJ number and the changes in uterine contractility were correlated with increased electrical and metabolic coupling. Evidence for the much smaller, but detectable, degree of electrical coupling in the preterm uterus is explained by the small (but again detectable) number of GJs present. In the intestine, GJs are readily detected in the circular muscle layer but have not been described in the adjacent longitudinal layer. While our immunohistochemical studies failed to detect GJs in the longitudinal layer, this may not be adequate to prove their absence. Therefore, current knowledge of GJ number and function is adequate to explain cell–cell coupling in the uterus. Although it remains uncertain whether GJs are absent from the longitudinal muscle of the intestine, there is no definitive evidence that cell–cell coupling can occur by means other than GJs.Key words: gap junctions, myometrium, connexins, smooth muscle, cell communication.

Treatment of EFA deficiency with dietary triglycerides or phospholipids in a murine model of extrahepatic cholestasis

2004 ◽  
Vol 286 (5) ◽  
pp. G822-G832 ◽  
Author(s):  
Anniek Werner ◽  
Rick Havinga ◽  
Folkert Kuipers ◽  
Henkjan J. Verkade
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Bile Duct Ligation ◽  
Murine Models ◽  
High Fat ◽  
Initial Value ◽  
Extrahepatic Cholestasis ◽  
Oral Supplementation ◽  
Duct Ligation ◽  
Long Chain

Essential fatty acid (EFA) deficiency during cholestasis is mainly due to malabsorption of dietary EFA ( 23 ). Theoretically, dietary phospholipids (PL) may have a higher bioavailability than dietary triglycerides (TG) during cholestasis. We developed murine models for EFA deficiency (EFAD) with and without extrahepatic cholestasis and compared the efficacy of oral supplementation of EFA as PL or as TG. EFAD was induced in mice by feeding a high-fat EFAD diet. After 3 wk on this diet, bile duct ligation was performed in a subgroup of mice to establish extrahepatic cholestasis. Cholestatic and noncholestatic EFAD mice continued on the EFAD diet (controls) or were supplemented for 3 wk with EFA-rich TG or EFA-rich PL. Fatty acid composition was determined in plasma, erythrocytes, liver, and brain. After 4 wk of EFAD diet, induction of EFAD was confirmed by a sixfold increased triene-to-tetraene ratio (T/T ratio) in erythrocytes of noncholestatic and cholestatic mice ( P < 0.001). EFA-rich TG and EFA-rich PL were equally effective in preventing further increase of the erythrocyte T/T ratio, which was observed in cholestatic and noncholestatic nonsupplemented mice (12- and 16-fold the initial value, respectively). In cholestatic mice, EFA-rich PL was superior to EFA-rich TG in decreasing T/T ratios of liver TG and PL (each P < 0.05) and in increasing brain PL concentrations of the long-chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid and arachidonic acid (each P < 0.05). We conclude that oral EFA supplementation in the form of PL is more effective than in the form of TG in increasing LCPUFA concentrations in liver and brain of cholestatic EFAD mice.

scholarly journals Influence of distal ileum exclusion on hepatic and renal functions in presence of extrahepatic cholestasis

2014 ◽  
Vol 41 (2) ◽  
pp. 112-116
Author(s):  
Evandro Luis de Oliveira Costa ◽  
Andy Petroianu ◽  
Geraldo Magela de Azevedo Júnior
Keyword(s):  
Terminal Ileum ◽  
Biliary Drainage ◽  
Hepatic Duct ◽  
Control Group ◽  
Extrahepatic Cholestasis ◽  
Functional Changes ◽  
Duct Ligation ◽  
Liver And Kidney ◽  
Group 3 ◽  
Group 1

OBJECTIVE: To verify whether the ileal exclusion interferes with liver and kidney functional changes secondary to extrahepatic cholestasis.METHODS: We studied 24 rats, divided into three groups with eight individuals each: Group 1 (control), Group 2 (ligation of the hepatic duct combined with internal biliary drainage), and Group 3 (bile duct ligation combined with internal biliary drainage and exclusion of the terminal ileum). Animals in Group 1 (control) underwent sham laparotomy. The animals of groups 2 and 3 underwent ligation and section of the hepatic duct and were kept in cholestasis for four weeks. Next, they underwent an internal biliary bypass. In Group 3, besides the biliary-enteric bypass, we associated the exclusion of the last ten centimeters of the terminal ileum and carried out an ileocolic anastomosis. After four weeks of monitoring, blood was collected from all animals of the three groups for liver and kidney biochemical evaluation (albumin, ALT, AST, direct and indirect bilirubin, alkaline phosphatase, cGT, creatinine and urea).RESULTS: there were increased values of ALT, AST, direct bilirubin, cGT, creatinine and urea in rats from Group 3 (p < 0.05).CONCLUSION: ileal exclusion worsened liver and kidney functions in the murine model of extrahepatic cholestasis, being disadvantageous as therapeutic procedure for cholestatic disorders.

scholarly journals The Lack of Nrf2 Causes Hepatocyte Dedifferentiation and Reduced Albumin Production in an Experimental Extrahepatic Cholestasis Model

2021 ◽  
Author(s):  
Guo-Ying Wang ◽  
Veronica Garcia ◽  
Joonyong Lee ◽  
Jennifer Yanum ◽  
Huaizhou Jiang ◽  
...  
Keyword(s):  
Epithelial Differentiation ◽  
Hepatocyte Proliferation ◽  
Sham Operation ◽  
Wild Type ◽  
Ductular Reaction ◽  
Extrahepatic Cholestasis ◽  
Liver Size ◽  
Duct Ligation ◽  
Albumin Production ◽  
In The Wild

AbstractThe transcription factor Nrf2 modulates the initiation and progression of a number of diseases including liver disorders. The aim of this study was to evaluate whether Nrf2 mediates hepatic adaptive responses to cholestasis. Wild-type and Nrf2-null mice were subjected to bile duct ligation (BDL) or a sham operation. Various assessments were performed at different days after surgery. Significant genotype-dependent changes in liver size, biliary ductular reaction, hepatocyte proliferation, and fibrotic response were not observed. However, as cholestasis progressed to Day 15 post-BDL, hepatocytes in the wild-type mice exhibited a tendency to dedifferentiate, indicated by the very weak expression of hepatic progenitor markers: CD133 and fibroblast growth factor-inducible 14 (Fn14). During the same period, Nrf2 deficiency augmented this tendency, manifested by higher CD133 expression, earlier, stronger, and continuous induction of Fn14 expression, and markedly reduced albumin production. Remarkably, as cholestasis advanced to the late stage (40 days after BDL), hepatocytes in the wild-type mice exhibited a Fn14+ phenotype and strikingly upregulated the expression of deleted in malignant brain tumor 1 (DMBT1), a protein essential for epithelial differentiation during development. In contrast, at this stage, hepatocytes in the Nrf2-null mice entirely inhibited the upregulation of DMBT1 expression, displayed a strong CD133+/Fn14+ phenotype indicative of severe dedifferentiation, and persistently reduced albumin production. Collectively, our studies revealed that Nrf2 maintains hepatocytes in the differentiated state potentially via the increased activity of the Nrf2/DMBT1 pathway during cholestasis. These findings enable us to gain novel insight into how hepatocytes respond to cholestasis.New and NoteworthyWe found that, when hepatocytes are exposed to cholestasis, they exhibit a tendency of dedifferentiation. In this case, Nrf2 is highly activated to markedly up-regulate the expression of epithelial differentiation gene DMBT1, which potentially prevent hepatocytes from dedifferentiation. Our findings revealed a plastic property of hepatocytes in response to cholestasis and demonstrated a novel Nrf2/DMBT1 pathway likely controlling this property of hepatocytes.

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