A quantitative freeze-fracture analysis of gap and tight junctions in the normal and cholestatic human liver

Robenek, Horst; Rassat, J; Themann, H

doi:10.1007/bf02892801

Cited by 29 publications

(5 citation statements)

References 30 publications

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“…Thin sections show intact tight junctions in infected L. lamottenii in spite of the dilated lumina. Similar observations have been reported in bile ductules Hollander and Schaffner, 1968a) and in hepatocytes (Metz et al, 1977;Robenek et al, 1981) of cholestatic livers. However, the observation in thin sections of preserved tight junctions does not exclude structural changes inside the junctional area and an increase in permeability of the canaliculo-sinusoidal barrier (Robenek et al, 1980).…”

Section: Figsupporting

confidence: 87%

Morphology of the bile ducts of the brook lamprey, Lampetra lamottenii (Le Sueur) before and during infection with the nematode, Truttaedacnitis stelmioides (Vessichelli, 1910) (Nematoda: Cucullanidae)

Eng

Youson

1992

Anat. Rec.

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Routine light microscopy and transmission and scanning electron microscopy were used to describe and compare the biliary tree of larval Lampetra lamottenii before and during infestation of the bile ducts with the nematode, Truttaedacnitis stelmioides. The most prominent changes to the biliary tree following infection by the parasite are the dilation of the bile ducts, alterations to their epithelial cells, and an increase in periductal fibrous tissue. In recently infected animals, the simple epithelium of dilated bile ducts often contains many mitotic figures. In long-term infestations, the epithelium is stratified or pseudostratified. Changes to the fine structure of the biliary epithelial cells include increase and/or dilation of the RER and SER, and increases in microfilaments, intermediate filaments, and microtubules. The abundance of dense bodies may reflect enhance reabsorption of biliary constituents, and their accumulation may ultimately result in cytolysis. There are increased mucous granules in the apical cytoplasm of biliary epithelial cells and an abundance of mucinous material within the bile duct lumen, and the basal lamina appears thickened. The changes to the liver of L. lamottenii following infection are discussed and compared to those reported in small mammals following bile duct ligation, in patients with extrahepatic biliary obstruction, and in parasitic infection of the biliary tree.

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Section: Figsupporting

confidence: 87%

Morphology of the bile ducts of the brook lamprey, Lampetra lamottenii (Le Sueur) before and during infection with the nematode, Truttaedacnitis stelmioides (Vessichelli, 1910) (Nematoda: Cucullanidae)

Eng

Youson

1992

Anat. Rec.

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“…A decrease in gap junction area or degradation of gap junction protein had possibly occurred in cholestatic livers, as has been shown in human liver [21] and in rat liver after bile duct ligation [22]. However, even taking this possibility into account, the decreased expression of the major liver gap junction protein (connexin 32) was not a general phenomenon in human HCCs, since one of the surrounding liver samples expressed as much connexin 32 mRNA as the two normal livers without observable pathological changes.…”

Section: Discussionmentioning

confidence: 82%

Aberrant expression of gap junction gene in primary human hepatocellular carcinomas: Increased expression of cardiac‐type gap junction gene connexin 43

Oyamada

Krutovskikh

Mesnil

et al. 1990

Molecular Carcinogenesis

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The expression of connexin 32 (the major liver gap junction protein) and connexin 43 (the major cardiac gap junction protein) was examined in six surgically removed human hepatocellular carcinoma tissues and the surrounding nontumorous livers using specific rat connexin probes. No decrease in connexin 32 mRNA expression was found in carcinomas compared with the surrounding nontumorous tissue. Morphometrical analysis also showed that in most of the carcinomas the number of gap junction spots stained with connexin 32 antibody was not less than that in the surrounding livers. These results are in striking contrast to the significant reductions in connexin 32 mRNA and protein expression observed in rat primary liver tumors induced by chemicals. On the other hand, all of the six human hepatocellular carcinomas exhibited elevated levels of connexin 43 mRNA, which was expressed at a very low level in the surrounding nontumorous livers. These carcinomas exhibited no detectable amplification of the connexin 43 gene. The present study suggests that gap junctional intercellular communication is altered in human hepatocellular carcinomas by molecular mechanisms different from those in rat hepatocarcinogenesis.

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“…Indeed, hemichannels not only are gap junction building blocks, but also provide a route for communication between the cytoplasm and the extracellular environment [75]. A similar type of channels is formed by pannexins (Panx), that are connexin-like proteins of which three family members have been characterized in humans [76], with Liver tissue from extrahepatic cholestasis patients~ Gap junctions [82,83] Liver tissue from cholelithiasis patients ↓ Gap junctions [84] Liver tissue from rats subjected to bile duct ligation ↓ Gap junctions [27,28] ↓ Gap junctions (ligation) ↑ Gap junctions (recanalization) [29] ↓ Cx32 protein (ligation) ↑ Cx32 protein (recanalization) [33] ↓ Cx32 protein (p38 MAPK-mediated) [32] ↓ GJIC ↓ Cx26 protein ↑ Cx26 mRNA ↓ Cx32 mRNA/protein [30] ↓ Cx26 protein ↓ Cx32 protein ↑ Cx43 protein [31] Liver tissue from rats treated with ethinyl estradiol~ Gap junctions [85] Cx26 protein ↑ Cx32 protein ~ Cx43 protein [31] Liver tissue from rats treated with estradiol valerate ↓ Gap junctions [86] Liver tissue from rats treated with phalloidin ↓ Gap junctions (pericentral) ↓ Cx32 protein [35] ↓ Cx26 protein ↓ Cx32 protein ~ Cx43 protein [31] Liver tissue from cdc42 ↓ Gap junctions [87] Liver tissue from lamprey undergoing biliary atresia ↓ Gap junctions [88] Primary rat hepatocyte doublet cultures exposed to taurolithocholic acid/taurolithocholicsulfate acid/ taurochenodeoxycholic acid ↓ GJIC [36] Normal rat cholangiocyte culture exposed to taurolithocholicsulfate acid ↓ GJIC [36] Liver tissue from rats subjected to choledochocaval fistula -deficient mice Panx1 and Panx2 being expressed in the liver [77]. Both hemichannels and pannexin channels are known to act as pathological pores, though specific information in relation to the liver is scarce [78].…”

Section: Discussionmentioning

confidence: 99%

Gap junctions and non-neoplastic liver disease

Vinken

2012

Journal of Hepatology

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Because of their critical role as goalkeepers of hepatic homeostasis, gap junctions are frequent targets in liver disease. This concept has been demonstrated on many occasions in the light of hepatocarcinogenesis. Relatively little focus has been put on the fate of gap junctions in other liver pathologies, including hepatitis, liver fibrosis and cirrhosis, cholestasis and hepatic ischemia and reperfusion injury. The present paper provides an in-depth description of the multiple changes in expression, localization and function of connexins, the molecular constituents of gap junctions. The use of connexins as biomarkers and therapeutic targets in liver disease is also illustrated.

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A quantitative freeze-fracture analysis of gap and tight junctions in the normal and cholestatic human liver

Cited by 29 publications

References 30 publications

Morphology of the bile ducts of the brook lamprey, Lampetra lamottenii (Le Sueur) before and during infection with the nematode, Truttaedacnitis stelmioides (Vessichelli, 1910) (Nematoda: Cucullanidae)

Morphology of the bile ducts of the brook lamprey, Lampetra lamottenii (Le Sueur) before and during infection with the nematode, Truttaedacnitis stelmioides (Vessichelli, 1910) (Nematoda: Cucullanidae)

Aberrant expression of gap junction gene in primary human hepatocellular carcinomas: Increased expression of cardiac‐type gap junction gene connexin 43

Gap junctions and non-neoplastic liver disease

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