Jauquicoa, C. (Carlos)

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2010 - 20112

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    Histological and ultrastructural comparison of cauterization and thrombosis stroke models in immune-deficient mice
    (BioMed Central, 2011) Casado-Nieto, M. (Maite); Romaguera-Ros, M. (Mirian); Gutierrez-Perez, M. (María); Gomez-Pinedo, U. (Ulises); Mora-Lee, S. (Silvia); Lopez, T. (Tania); Garcia-Verdugo, J.M. (José Manuel); Jauquicoa, C. (Carlos); Sirerol-Piquer, M.S. (María Salomé); Prosper-Cardoso, F. (Felipe); Abizanda-Sarasa, G. (Gloria)
    Background: Stroke models are essential tools in experimental stroke. Although several models of stroke have been developed in a variety of animals, with the development of transgenic mice there is the need to develop a reliable and reproducible stroke model in mice, which mimics as close as possible human stroke. Methods: BALB/Ca-RAG2-/-gc-/- mice were subjected to cauterization or thrombosis stroke model and sacrificed at different time points (48hr, 1wk, 2wk and 4wk) after stroke. Mice received BrdU to estimate activation of cell proliferation in the SVZ. Brains were processed for immunohistochemical and EM. Results: In both stroke models, after inflammation the same glial scar formation process and damage evolution takes place. After stroke, necrotic tissue is progressively removed, and healthy tissue is preserved from injury through the glial scar formation. Cauterization stroke model produced unspecific damage, was less efficient and the infarct was less homogeneous compared to thrombosis infarct. Finally, thrombosis stroke model produces activation of SVZ proliferation. Conclusions: Our results provide an exhaustive analysis of the histopathological changes (inflammation, necrosis, tissue remodeling, scarring...) that occur after stroke in the ischemic boundary zone, which are of key importance for the final stroke outcome. This analysis would allow evaluating how different therapies would affect wound and regeneration. Moreover, this stroke model in RAG 2-/- gC -/- allows cell transplant from different species, even human, to be analyzed.
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    Sustained release of VEGF through PLGA microparticles improves vasculogenesis and tissue remodeling in an acute myocardial ischemia–reperfusion model
    (Elsevier, 2010) Blanco-Prieto, M.J. (María José); Gavira, J.J. (Juan José); Ortiz-de-Solorzano, C. (Carlos); Tamayo, E. (Esther); Mazo, M. (Manuel); Jauquicoa, C. (Carlos); Garbayo, E; Prosper-Cardoso, F. (Felipe); Formiga, F.R. (Fabio R.); Pelacho, B. (Beatriz); Simon-Yarza, T. (Teresa); Abizanda-Sarasa, G. (Gloria)
    The use of pro-angiogenic growth factors in ischemia models has been associated with limited success in the clinical setting, in part owing to the short lived effect of the injected cytokine. The use of a microparticle system could allow localized and sustained cytokine release and consequently a prolonged biological effect with induction of tissue revascularization. To assess the potential of VEGF165 administered as continuous release in ischemic disease, we compared the effect of delivery of poly(lactic–co-glycolic acid) (PLGA) microparticles (MP) loaded with VEGF165 with free-VEGF or control empty microparticles in a rat model of ischemia–reperfusion. VEGF165 loaded microparticles could be detected in the myocardium of the infarcted animals for more than a month after transplant and provided sustained delivery of active protein in vitro and in vivo. One month after treatment, an increase in angiogenesis (small caliber caveolin-1 positive vessels) and arteriogenesis (α-SMA-positive vessels) was observed in animals treated with VEGF microparticles (pb0.05), but not in the empty microparticles or free-VEGF groups. Correlating with this data, a positive remodeling of the heart was also detected in the VEGF-microparticle group with a significantly greater LV wall thickness (pb0.01). In conclusion, PLGA microparticle is a feasible and promising cytokine delivery system for treatment of myocardial ischemia. This strategy could be scaled up and explored in pre-clinical and clinical studies.