Full metadata record
DC Field | Value | Language |
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dc.creator | Bustos, M. (Matilde) | - |
dc.creator | Beraza, N. (Naiara) | - |
dc.creator | Lasarte, J.J. (Juan José) | - |
dc.creator | Baixeras, E. (Elena) | - |
dc.creator | Alzuguren, P. (Pilar) | - |
dc.creator | Bordet, T. (Thierry) | - |
dc.creator | Prieto, J. (Jesús) | - |
dc.date.accessioned | 2012-01-16T08:14:35Z | - |
dc.date.available | 2012-01-16T08:14:35Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Bustos M, Beraza N, Lasarte JJ, Baixeras E, Alzuguren P, Bordet T, et al. Protection against liver damage by cardiotrophin-1: a hepatocyte survival factor up-regulated in the regenerating liver in rats. Gastroenterology 2003 Jul;125(1):192-201. | es_ES |
dc.identifier.issn | 0016-5085 | - |
dc.identifier.uri | https://hdl.handle.net/10171/20422 | - |
dc.description.abstract | BACKGROUND & AIMS: Cardiotrophin-1 (CT-1) is a member of the interleukin 6 (IL-6) family of cytokines, which protect cardiac myocytes against thermal and ischemic insults. In this study, we investigated the expression of CT-1 by liver cells and its possible hepatoprotective properties. METHODS: We analyzed the production, signaling, and antiapoptotic properties of CT-1 in hepatocytes and the expression of this cytokine during liver regeneration. We also investigated whether CT-1 might exert protective effects in animal models of liver damage. RESULTS: We found that CT-1 is up-regulated during liver regeneration and exerts potent antiapoptotic effects on hepatocytic cells. Hepatocytes cultured under serum starvation or stimulated with the pro-apoptotic cytokine transforming growth factor beta (TGF-beta) produce CT-1, which behaves as an autocrine/paracrine survival factor. Treatment with an adenovirus encoding CT-1 efficiently protects rats against fulminant liver failure after subtotal hepatectomy, an intervention that causes 91% mortality in control animals whereas 54% of those receiving CT-1 gene therapy were long-term survivors. This protective effect was associated with reduced caspase-3 activity and activation of the antiapoptotic signaling cascades signal transducer and activator of transcription (Stat-3), extracellular regulated kinases (Erk) 1/2, and Akt in the remnant liver. Gene transfer of CT-1 to the liver also abrogated Concanavalin A (Con-A) liver injury and activated antiapoptotic pathways in the hepatic tissue. Similar protection was obtained by treating the animals with 5 microg of recombinant CT-1 given intravenously before Con-A administration. CONCLUSIONS: We show that CT-1 is a hepatocyte survival factor that efficiently reduces hepatocellular damage in animal models of acute liver injury. Our data point to CT-1 as a new promising hepatoprotective therapy. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Wb saunders | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | Cytokines/genetics | es_ES |
dc.subject | Cytokines/pharmacology | es_ES |
dc.subject | Gene Therapy | es_ES |
dc.subject | Liver Failure/drug therapy | es_ES |
dc.title | Protection against liver damage by cardiotrophin-1: a hepatocyte survival factor up-regulated in the regenerating liver in rats | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
dc.identifier.doi | http://dx.doi.org/10.1016/S0016-5085(03)00698-X | es_ES |
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