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http://purl.uniprot.org/citations/17681181http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17681181http://www.w3.org/2000/01/rdf-schema#comment"

Background and aims

Hepatic regeneration is a heterogeneous phenomenon involving several cell populations. Oval cells are considered liver stem cells, a portion of which derive from bone marrow (BM). Recent studies have shown that granulocyte-colony stimulating factor (G-CSF) may be effective in facilitating liver repair. However, it remains unclear if G-CSF acts by mobilizing BM cells, or if it acts locally within the liver microenvironment to facilitate the endogenous restoration program. In the present study, we assessed the involvement of G-CSF during oval cell activation.

Methods

Dipeptidyl-peptidase-IV-deficient female rats received BM transplants from wild-type male donors. Four weeks later, rats were subjected to the 2-acetylaminofluorene/partial hepatectomy model of oval cell-mediated liver regeneration, followed by administration of either nonpegylated G-CSF or pegylated G-CSF. Control animals did not receive further treatments after surgery. The magnitude of oval cell reaction, the entity of BM contribution to liver repopulation, as well as the G-CSF/G-CSF-receptor expression levels were evaluated. In addition, in vitro proliferation and migration assays were performed on freshly isolated oval cells.

Results

Oval cells were found to express G-CSF receptor and G-CSF was produced within the regenerating liver. G-CSF administration significantly increased both the magnitude of the oval cell reaction, and the contribution of BM to liver repair. Finally, G-CSF acted as a chemoattractant and a mitogen for oval cells in vitro.

Conclusions

We have shown that G-CSF facilitates hepatic regeneration by increasing the migration of BM-derived progenitors to the liver, as well as enhancing the endogenous oval cell reaction."xsd:string
http://purl.uniprot.org/citations/17681181http://purl.org/dc/terms/identifier"doi:10.1053/j.gastro.2007.05.018"xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/author"Oh S.H."xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/author"Petersen B.E."xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/author"Gasbarrini A."xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/author"Shupe T.D."xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/author"Piscaglia A.C."xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/name"Gastroenterology"xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/pages"619-631"xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/title"Granulocyte-colony stimulating factor promotes liver repair and induces oval cell migration and proliferation in rats."xsd:string
http://purl.uniprot.org/citations/17681181http://purl.uniprot.org/core/volume"133"xsd:string
http://purl.uniprot.org/citations/17681181http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17681181
http://purl.uniprot.org/citations/17681181http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17681181
http://purl.uniprot.org/uniprot/#_A6HIT8-mappedCitation-17681181http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17681181
http://purl.uniprot.org/uniprot/#_P97712-mappedCitation-17681181http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17681181
http://purl.uniprot.org/uniprot/P97712http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17681181
http://purl.uniprot.org/uniprot/A6HIT8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17681181