Expression and regulation of gap junctions in rat cholangiocytes

Bode, Hans-Peter; Wang, Lifu; Cassio, Doris; Leite, M. Fátima; St‐Pierre, Marie V.; Hirata, Keiji; Okazaki, Keisuke; Sears, Marvin L.; Meda, Paolo; Nathanson, Michael H.; Dufour, Jean–François

doi:10.1053/jhep.2002.35274

Cited by 68 publications

(54 citation statements)

References 53 publications

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“…In line with this observation is the fi nding that Cx32 knock-out mice show lowered blood glucose levels upon glycogenolytic stimulation (Stumpel et al, 1998). A similar scenario is seen in bile formation and fl ow, whereby ductular secretion from cholangiocytes depends on the spread of calcium waves through Cx43-containing gap junctions (Bode et al, 2002;Nathanson et al, 1999).…”

Section: Connexins and Liver Organogenesismentioning

confidence: 84%

Modifications in Connexin Expression in Liver Development and Cancer

Vinken

Kock

Oliveira

et al. 2012

Cell Communication & Adhesion

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The establishment of an elaborate gap junctional intercellular communication network, especially between hepatocytes, is important for normal liver development. In fact, the production of the gap junction building blocks, the connexins, undergoes several well-defi ned changes throughout the hepatic differentiation process. This ultimately results in the acquisition of an adult connexin expression pattern which is critical for maintaining the fully differentiated hepatocyte-specifi c phenotype. Abnormalities of connexin production are observed in a number of pathological conditions, such as during liver cancer. This article provides an overview of these processes with emphasis on the underlying molecular mechanisms.

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Section: Connexins and Liver Organogenesismentioning

confidence: 84%

Modifications in Connexin Expression in Liver Development and Cancer

Vinken

Kock

Oliveira

et al. 2012

Cell Communication & Adhesion

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“…The intercellular junctions are shown to be dramatically altered under obstructive cholestasis; for example, the level of connexins decreases (Fallon et al 1995). Connexins 32 and 43 are the main proteins of gap junctions of hepatocytes and cholangiocytes respectively (Bode et al 2002, Fallon et al 1995. Prolactin has been shown to increase connexin levels for example, connexin 32 in mammary gland (Miyoshi et al 2001) and connexin 43 in pancreas islets (Collares-Buzato et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Long isoform of prolactin receptor predominates in rat intrahepatic bile ducts and further increases under obstructive cholestasis

Bogorad

Ostroukhova²,

Orlova³

et al. 2006

Journal of Endocrinology

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Prolactin participates in the regulation of liver function. However, prolactin receptor (PrlR) expression and its regulation have been described only for hepatocytes. In this study, we investigated the expression and regulation of PrlR isoforms in the other important intrahepatic cellular compartment: the biliary epithelial cells, or cholangiocytes. Our aim was to determine whether prolactin should be considered as a potential regulator of cholangiocyte function under normal and pathological conditions. Cholangiocytes and hepatocytes were differentially isolated from rat liver. PrlR expression was analysed at the mRNA level by isoform-specific semiquantitative PCR, and at the protein level by immunostaining of liver sections. Hormonal regulation of PrlR expression was evaluated by comparing intact rats with gonadectomized, pituitary-grafted or bromocriptine-treated animals. Common bile-duct ligation was used as the experimental model of cholestasis. Our results demonstrate that the expression pattern and regulation of PrlR isoforms is totally different in cholangiocytes compared with hepatocytes: (1) mature rat cholangiocytes express low levels of PrlR, while it is very high in hepatocytes, (2) only the long isoform is detected in cholangiocytes, while the short isoform predominates in hepatocytes and (3) PrlR levels in cholangiocytes are induced by obstructive cholestasis, but not by sex hormones or prolactin, while it is the opposite in hepatocytes. From these data, the actions of prolactin on liver are anticipated to exhibit strong cell-type specificity in both normal and pathological conditions.

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“…Hepatocytes express connexin 32 in normal liver, whereas cells of the biliary system express connexin 43. 22 Oval cells were positive for connexin 43, but this protein was not present in the newly differentiated small hepatocytes (Fig. 5B).…”

Section: Characteristic Changes In Differentiation Markersmentioning

confidence: 95%

2-acetylaminofluorene dose-dependent differentiation of rat oval cells into hepatocytes: Confocal and electron microscopic studies

et al. 2004

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The 2-acetylaminofluorene (AAF)/partial hepatectomy (PH) model is one of the most extensively studied experimental systems for oval cell proliferation and differentiation. We have previously described the oval cells as forming ductular structures surrounded by basement membrane, representing extensions of the canals of Hering. Herein we analyze the differentiation of oval cells into hepatocytes after varying degrees of liver damage induced by AAF. At a low dose of AAF, most oval cells synchronously differentiate into small hepatocytes by 6 days after the PH, resulting in complete restoration of the liver structure in 10 days. Higher doses of AAF delay the differentiation process and the new hepatocytes form foci, in contrast to what is observed at the low dose. Qualitatively, the differentiation process seems to be identical at the cellular level under both conditions. The transition from the expanding oval cell population into hepatocytes was correlated with the upregulation of hepatocyte nuclear factor 4 and the disappearance of the basement membrane. Also, the differentiation of oval cells into hepatocytes coincided with the loss of alpha-fetoprotein and OV-6 staining, and the replacement of the biliary cell-specific ␣6 integrin and connexin 43 with the hepatocyte-specific ␣1 integrin and connexin 32. In addition, bile canaliculi form between the new hepatocytes. In conclusion, these results indicate the rate of oval cell differentiation into hepatocytes is context dependent and suggest that, under favorable conditions, oval cells can complete this process much faster than previously appreciated.

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Expression and regulation of gap junctions in rat cholangiocytes

Cited by 68 publications

References 53 publications

Modifications in Connexin Expression in Liver Development and Cancer

Modifications in Connexin Expression in Liver Development and Cancer

Long isoform of prolactin receptor predominates in rat intrahepatic bile ducts and further increases under obstructive cholestasis

2-acetylaminofluorene dose-dependent differentiation of rat oval cells into hepatocytes: Confocal and electron microscopic studies

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