Basic-liver, pancreas, and biliary tractAmphiregulin: An early trigger of liver regeneration in mice
Section snippets
Patients
Liver tissue samples were from 2 groups of subjects. The first group comprised control individuals (n = 26; 19 men; mean age, 50.8 years; range, 18–73 years) with normal or minimal changes in the liver. We collected tissue samples at surgery (16 cases) of digestive tumors or from percutaneous liver biopsy performed because of mild alteration of liver function tests (10 cases). The second group comprised subjects with liver cirrhosis (n = 29; 24 men; mean age, 56 years; range, 36–77 years) that
Amphiregulin gene expression is induced in human and experimental liver injury
We have previously shown that expression of the transcription factor WT1 is induced in almost all tested samples of cirrhotic human liver and always in CCl4-induced cirrhosis in rats.5 The fact that AR is a major transcriptional target for WT17 led us to examine the expression of this growth factor in the liver of cirrhotic patients. Although real-time PCR analysis showed barely detectable levels of AR expression in healthy human liver, AR gene expression was observed in approximately 75% of
Discussion
The loss of functional liver mass induced by toxins, viral infections, or tissue resection triggers a well-orchestrated regenerative response that involves a number of cytokines, growth factors, hormones, and metabolites.1, 2, 3, 4 The identities of many of these factors have been established over the past decades, but the complexity of this response likely involves additional players. Here we provide several lines of evidence supporting AR, a ligand of the EGF-R, as a new factor involved in
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This work was supported by the agreement between Fundación Investigación Médica Aplicada (FIMA) and the “Unión Temporal de Empresas (UTE) project CIMA,” Grants C03/02 and G03/015 from Instituto de Salud Carlos III (C.B., E.R.G.-T., J.P., M.A.A.), Grant SAF-2004-03538 (M.A.A.), National Institutes of Health Grants CA49793 and CA43793 (D.C.L.), and Grant FISPI040819 from Ministerio de Sanidad (to C. B.). E.E. is supported by a fellowship from Gobierno de Navarra, Spain.
- 1
Address correspondence to: Matias A. Avila, PhD, Division of Hepatology and Gene Therapy, CIMA, Universidad de Navarra, 31008 Pamplona, Spain. e-mail: [email protected]; fax: (34) 948-194717.
- 2
J.P. and M.A.A. share senior authorship.