6533b853fe1ef96bd12ac38b
RESEARCH PRODUCT
Beta-2-glycoprotein I is growth regulated and plays a role as survival factor for hepatocytes
Gianluca ParavizziniG. MarinoMaria Antonietta RagusaCarlo M. BarbagalloGaetano MagroMaurizio AvernaDavide NotoAngelo B. CefalùMaria Clorinda MazzarinoAlberto NotarbartoloDaniela CallariGiovanni EmmanueleSalvatore TravaliGiovanni Bartolonisubject
medicine.medical_specialtyRegenerating liverSurvivalCell SurvivalCell cycle expressionCellCell Culture TechniquesButyrateBiologyBiochemistrychemistry.chemical_compoundAlbuminsInternal medicineGene expressionmedicineAnimalsHumansBeta 2-Glycoprotein IRats WistarGlycoproteinsAlbuminSodium butyrateCell BiologyLiver RegenerationRatsBeta-2-glycoprotein ICell biologyButyratesEndocrinologymedicine.anatomical_structureGene Expression RegulationLiverchemistrybeta 2-Glycoprotein IHepatocytesApolipoprotein HHepatic stellate cellGDF15description
Beta-2-glycoprotein I (beta(2)GPI) is mainly produced by the liver and is found in plasma partially associated to lipoproteins. Although various properties have been attributed to this protein, its physiological role remains still unclear. We investigated its expression in cultured liver cells and in regenerating liver. Expression studies in HepG2 cells demonstrate that beta(2)GPI mRNA is regulated in a cell cycle-dependent manner, with very low expression in low cycling conditions and increasing levels in proliferating cells. p21 WAF-dependent growth arrest, induced by butyrate treatment, down-regulate beta(2)GPI mRNA levels. Immunolocalization in normal rat liver shows a non-homogeneous pattern, being mainly present in the centrolobular area; post-hepatectomy regenerating rat liver is uniformly immunostained and mitotic elements show the highest protein expression. Albumin gene expression, studies as control liver specific product, was not affected by sodium butyrate induced growth arrest. As previously reported for endothelial cells, beta(2)GPI behaves as survival factor for HepG2 cells: when increasing amounts of the protein (10-50 microg) have been added to serum deficient cultured liver cells a progressive reduced cell loss was observed. In conclusion, the present data demonstrate that beta(2)GPI gene expression is strictly related to the proliferative status of hepatic cells and that this protein could play a role in maintaining liver cells vitality when exposed to different stress factors such as regeneration after partial hepatectomy or growth factors depletion.
year | journal | country | edition | language |
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2004-01-01 | The International Journal of Biochemistry & Cell Biology |