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- Arroyo-Torres, B., et al.
(författare)
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VLTI/AMBER observations of cold giant stars: atmospheric structures and fundamental parameters
- 2014
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Ingår i: Astronomy and Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 566
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Tidskriftsartikel (refereegranskat)abstract
- Aims. The main goal of this research is to determine the angular size and the atmospheric structures of cool giant stars (epsilon Oct, beta Peg, NU Pav, psi Peg, and gamma Hya) and to compare them with hydrostatic stellar model atmospheres, to estimate the fundamental parameters, and to obtain a better understanding of the circumstellar environment. Methods. We conducted spectro-interferometric observations of epsilon Oct, beta Peg, NU Pav, and psi Peg in the near-infrared K band (2.13-2.47 mu m), and gamma Hya (1.9-2.47 mu m) with the VLTI/AMBER instrument at medium spectral resolution (similar to 1500). To obtain the fundamental parameters, we compared our data with hydrostatic atmosphere models (PHOENIX). Results. We estimated the Rosseland angular diameters of epsilon Oct, beta Peg, NU Pav, psi Peg, and gamma Hya to be 11.66 +/- 1.50 mas, 16.87 +/- 1.00 mas, 13.03 +/- 1.75 mas, 6.31 +/- 0.35 mas, and 3.78 +/- 0.65 mas, respectively. Together with distances and bolometric fluxes (obtained from the literature), we estimated radii, effective temperatures, and luminosities of our targets. In the beta Peg visibility, we observed a molecular layer of CO with a size similar to that modeled with PHOENIX. However, there is an additional slope in absorption starting around 2.3 m. This slope is possibly due to a shell of H2O that is not modeled with PHOENIX (the size of the layer increases to about 5% with respect to the near-continuum level). The visibility of psi Peg shows a low increase in the CO bands, compatible with the modeling of the PHOENIX model. The visibility data of epsilon Oct, NU Pav, and gamma Hya show no increase in molecular bands. Conclusions. The spectra and visibilities predicted by the PHOENIX atmospheres agree with the spectra and the visibilities observed in our stars (except for beta Peg). This indicates that the opacity of the molecular bands is adequately included in the model, and the atmospheres of our targets have an extension similar to the modeled atmospheres. The atmosphere of beta Peg is more extended than that predicted by the model. The role of pulsations, if relevant in other cases and unmodeled by PHOENIX, therefore seems negligible for the atmospheric structures of our sample. The targets are located close to the red limits of the evolutionary tracks of the STAREVOL model, corresponding to masses between 1 M-circle dot and 3 M-circle dot. The STAREVOL model fits the position of our stars in the Hertzsprung-Russell (HR) diagram better than the Ekstrom model does. STAREVOL includes thermohaline mixing, unlike the Ekstrom model, and complements the latter for intermediate-mass stars.
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| 2. |
- Moreno-Càceres, J, et al.
(författare)
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Caveolin-1 is required for TGF-β-induced transactivation of the EGF receptor pathway in hepatocytes through the activation of the metalloprotease TACE/ADAM17
- 2014
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Ingår i: Cell Death and Disease. - : Springer Science and Business Media LLC. - 2041-4889 .- 2041-4889. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- Transforming growth factor-beta (TGF-β) plays a dual role in hepatocytes, inducing both pro- and anti-apoptotic responses, whose balance decides cell fate. Survival signals are mediated by the epidermal growth factor receptor (EGFR) pathway, which is activated by TGF-β in these cells. Caveolin-1 (Cav1) is a structural protein of caveolae linked to TGF-β receptors trafficking and signaling. Previous results have indicated that in hepatocytes, Cav1 is required for TGF-β-induced anti-apoptotic signals, but the molecular mechanism is not fully understood yet. In this work, we show that immortalized Cav1(-/-) hepatocytes were more sensitive to the pro-apoptotic effects induced by TGF-β, showing a higher activation of caspase-3, higher decrease in cell viability and prolonged increase through time of intracellular reactive oxygen species (ROS). These results were coincident with attenuation of TGF-β-induced survival signals in Cav1(-/-) hepatocytes, such as AKT and ERK1/2 phosphorylation and NFκ-B activation. Transactivation of the EGFR pathway by TGF-β was impaired in Cav1(-/-) hepatocytes, which correlated with lack of activation of TACE/ADAM17, the metalloprotease responsible for the shedding of EGFR ligands. Reconstitution of Cav1 in Cav1(-/-) hepatocytes rescued wild-type phenotype features, both in terms of EGFR transactivation and TACE/ADAM17 activation. TACE/ADAM17 was localized in detergent-resistant membrane (DRM) fractions in Cav1(+/+) cells, which was not the case in Cav1(-/-) cells. Disorganization of lipid rafts after treatment with cholesterol-binding agents caused loss of TACE/ADAM17 activation after TGF-β treatment. In conclusion, in hepatocytes, Cav1 is required for TGF-β-mediated activation of the metalloprotease TACE/ADAM17 that is responsible for shedding of EGFR ligands and activation of the EGFR pathway, which counteracts the TGF-β pro-apoptotic effects. Therefore, Cav1 contributes to the pro-tumorigenic effects of TGF-β in liver cancer cells.
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