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Title

Transforming growth factor-beta activates both pro-apoptotic and survival signals in fetal rat hepatocytes

AuthorsValverde, Ángela M.; Herrera, Blanca; Sánchez, Aránzazu; Benito, Manuel; Fernández, Margarita ; Fabregat, Isabel
KeywordsApoptosis
TGF-β
Phosphatidylinositol 3-kinase
Akt
Reactive oxygen species
Caspases
Hepatocytes
Issue Date2004
PublisherElsevier
CitationExperimental Cell Research 292(1): 209-218 (2004)
AbstractTransforming growth factor-beta (TGF-β) induces apoptosis in fetal rat hepatocytes. However, a subpopulation of these cells survives concomitant with changes in morphology and phenotype, reminiscent of an epithelial mesenchymal transition (EMT) [Exp. Cell Res. 252 (1999) 281–291]. In this work, we have isolated the subpopulation that survives to TGF-β-induced apoptosis, showing that these cells maintain the response to TGF-β in terms of Smads activation and growth inhibition. Analyses of the intracellular signals that could impair the apoptotic effects of TGF-β have indicated that the phosphatidylinositol 3-kinase (PI 3-K)/Akt pathway is activated in these resistant cells. Experiments in fetal rat hepatocytes have shown that TGF-β is able to transiently activate PI 3-K/Akt by a mechanism independent of protein synthesis but dependent on a tyrosine kinase activity. Pro-apoptotic signals, such as oxidative stress and caspases, contribute to the loss of Akt at later times. Inhibiting PI 3-K sensitizes fetal hepatocytes (FH) to the apoptosis induced by TGF-β and causes spontaneous death in the resistant cells. In conclusion, TGF-β, as it is known for other cytokines, could be inducing pro-apoptotic and survival signals in hepatocytes, the balance among them will decide cell fate.
URIhttp://hdl.handle.net/10261/152527
DOI10.1016/j.yexcr.2003.08.015
Identifiersdoi: 10.1016/j.yexcr.2003.08.015
issn: 0014-4827
e-issn: 1090-2422
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