Nuestros investigadores

Idoia Belza Zuazu

Publicaciones científicas más recientes (desde 2010)

Autores: Fernandez-Robredo, P; Recalde, Sergio; Hernandez, M.; et al.
Revista: INVESTIGATIVE OPHTHALMOLOGY AND VISUAL SCIENCE
ISSN 0146-0404  Vol. 60  Nº 9  2019 
Autores: Recalde, Sergio; Hernandez, M.; et al.
Revista: INVESTIGATIVE OPHTHALMOLOGY AND VISUAL SCIENCE
ISSN 0146-0404  Vol. 60  Nº 9  2019 
Autores: Hernandez, M.; Fernandez-Robredo, P; Recalde, Sergio; et al.
Revista: INVESTIGATIVE OPHTHALMOLOGY AND VISUAL SCIENCE
ISSN 0146-0404  Vol. 60  Nº 9  2019 
Autores: Recalde, Sergio; Hernández, María; Bezunartea, J.; et al.
Revista: INVESTIGATIVE OPHTHALMOLOGY AND VISUAL SCIENCE
ISSN 0146-0404  Vol. 59  Nº 9  2018 
Autores: Fernandez-Robredo, P; Hernández, María; Recalde, Sergio; et al.
Revista: INVESTIGATIVE OPHTHALMOLOGY AND VISUAL SCIENCE
ISSN 0146-0404  Vol. 58  Nº 8  2017 
Autores: Fernandez-Robredo, P; Saenz-de-Viteri, Manuel; Recalde, Sergio; et al.
Revista: INVESTIGATIVE OPHTHALMOLOGY AND VISUAL SCIENCE
ISSN 0146-0404  Vol. 57  Nº 12  2016  págs. 3363
Purpose : To evaluate intracellular accumulation and the effect of bevacizumab, ranibizumab and aflibercept on cellular migration and permeability in a human retinal pigmented epithelium (RPE) cell line. Methods : Experiments were performed on ARPE-19 cells and anti-VEGF drugs were diluted to a concentration equivalent to their clinical doses. Anti-VEGFs were labeled with Alexa 488 fluorochrome to detect intracellular accumulation by flow cytometry at 1 hour, 1 day and five days. Further, transepithelial electrical resistance (TEER) was measured in transwells at 2, 4, 6, 12 and 24 hours to assess the effect of anti-VEGFs on RPE permeability. Moreover, TEER was also measured at the same time points in the presence of different doses of H2O2 to replicate the oxidative environment observed in Age-related Macular Degeneration (AMD). Wound healing was assessed to determine the effect of the drugs on cellular migration during 72 hours to measured cell covered area by ImageJ software. Results : The three studied drugs were observed to accumulate inside the cells and they were still detectable five days after being added (p<0.001). A dose-dependent increased in cell permeability was observed in cells treated with H2O2 (p<0.05) that was reverted from the time point of 12 hours and became non-significant. Anti-VEGF drugs did not affect the permeability along time and they were able to reduce the effect of H2O2. Cells treated with anti-VEGF drugs at the beginning of the experiment showed a significant decrease in the damage produced by H2O2 at 4, 6 and 12 hours (p<0.05) with no significant difference between the treatments. On the contrary, when anti-VEGF treatment was used 6 hours after the beginning of the experiment, none of the 3 drugs decreased the deleterious effect of H2O2 in TEER. Anti-VEGF drugs did not affect cellular migration. Conclusions : Intracellular accumulation of bevacizumab, ranibizumab and aflibercept does not seem to be toxic or affect cell permeability and migration. Moreover, our study suggests that anti-VEGFs have a positive effect on the barrier function of the RPE.
Autores: Belza, Idoia; et al.
Revista: ONCOIMMUNOLOGY
ISSN 2162-4011  Vol. 1  Nº 9  2012  págs. 1527-36
Cardiotrophin-1 (CT-1/CTF1) is a member of the interleukin-6 (IL-6) family of cytokines that stimulates STAT-3 phosphorylation in cells bearing the cognate receptor. We report that Ctf1(-/-) mice (hereby referred to as CT-1(-/-) mice) are resistant to the hepatic engraftment of MC38 colon carcinoma cells, while these cells engraft normally in the mouse subcutaneous tissue. Tumor intake in the liver could be enhanced by the systemic delivery of a recombinant adenovirus encoding CT-1, which also partly rescued the resistance of CT-1(-/-) mice to the hepatic engraftment of MC38 cells. Moreover, systemic treatment of wild-type (WT) mice with a novel antibody-neutralizing mouse CT-1 also reduced engraftment of this model. Conversely, experiments with Panc02 pancreatic cancer and B16-OVA melanoma cells in CT-1(-/-) mice revealed rates of hepatic engraftment similar to those observed in WT mice. The mechanism whereby CT-1 renders the liver permissive for MC38 metastasis involves T lymphocytes and natural killer (NK) cells, as shown by selective depletion experiments and in genetically deficient mice. However, no obvious changes in the number or cell killing capacity of liver lymphocytes in CT-1(-/-) animals could be substantiated. These findings demonstrate that the seed and soil concept to understand metastasis can be locally influenced by cytokines as well as by the cellular immune system