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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2006-7-25
pubmed:abstractText
Gap junctions between murine hepatocytes are composed of two subunit proteins, connexin26 (Cx26) and connexin32 (Cx32). Previously, we found increased formation of chemically induced liver tumours but no increase in spontaneous development of preneoplastic hepatic foci in mice that lacked Cx32 and expressed decreased amounts of Cx26. In order to clarify this tumour-suppressive effect and to overcome embryonic lethality of constitutive Cx26-deficient mice, cell type-specific targeting of the Cx26 gene was performed. Mice with loxP-flanked Cx26 coding DNA were crossed with mice expressing the Cre recombinase exclusively in hepatocytes. Progeny mice lacking Cx26 in the liver were viable and fertile with no obvious signs of phenotypic alterations. To generate mice that totally lack gap junctional intercellular coupling, these mice were crossed with constitutive Cx32-deficient mice. We found no increase in spontaneously induced liver tumour formation in Cx26 and double deficient Cx26/Cx32 mice. Occasionally, double deficient livers exhibited morphological alterations, like amyloidosis, and a slightly increased basal proliferation rate of hepatocytes. Although the absence of gap junction channels led to altered expression of adhesion-related proteins like E-cadherin and actin, microarray analyses of total liver transcripts yielded only few differences between Cx26-deficient and double deficient livers compared to control samples. Our results suggest that total lack of gap junctional communication due to hepatocytic ablation of Cx26 and Cx32 does not drastically alter basal hepatocytic function and does not lead to increased spontaneous liver tumour formation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0171-9335
pubmed:author
pubmed:issnType
Print
pubmed:volume
85
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
717-28
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16740338-Animals, pubmed-meshheading:16740338-Apoptosis, pubmed-meshheading:16740338-Carcinogens, pubmed-meshheading:16740338-Cell Communication, pubmed-meshheading:16740338-Cell Proliferation, pubmed-meshheading:16740338-Connexins, pubmed-meshheading:16740338-Diethylnitrosamine, pubmed-meshheading:16740338-Female, pubmed-meshheading:16740338-Gap Junctions, pubmed-meshheading:16740338-Hepatocytes, pubmed-meshheading:16740338-Homeostasis, pubmed-meshheading:16740338-Immunoblotting, pubmed-meshheading:16740338-Immunohistochemistry, pubmed-meshheading:16740338-Liver, pubmed-meshheading:16740338-Liver Neoplasms, Experimental, pubmed-meshheading:16740338-Male, pubmed-meshheading:16740338-Mice, pubmed-meshheading:16740338-Mice, Transgenic, pubmed-meshheading:16740338-Oligonucleotide Array Sequence Analysis
pubmed:year
2006
pubmed:articleTitle
Ablation of gap junctional communication in hepatocytes of transgenic mice does not lead to disrupted cellular homeostasis or increased spontaneous tumourigenesis.
pubmed:affiliation
Institut für Genetik, Abteilung Molekulargenetik, Universität Bonn, Römerstr. 164, D-53117 Bonn, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't