Browsing by Author "Riquelme, Jaime A."

Now showing 1 - 7 of 7
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    Angiotensin II-Regulated Autophagy Is Required for Vascular Smooth Muscle Cell Hypertrophy
    (2019) Mondaca-Ruff, David; Riquelme, Jaime A.; Quiroga Lagos, Clara Rosa; Norambuena-Soto, Ignacio; Sanhueza-Olivares, Fernanda; Villar-Fincheira, Paulina; Hernández-Díaz,Tomás; Cancino-Arenas, Nicole; San Martín, Alejandra; García, Lorena; Lavandero, Sergio; Chiong, Mario
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    Counter-regulatory renin–angiotensin system in cardiovascular disease
    (2019) Ocaranza, María Paz; Riquelme, Jaime A.; García, Lorena; Jalil Milad, Jorge; Chiong, Mario; Santos, Robson A. S.; Lavandero, Sergio
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    Enfermedades cardiovasculares y cáncer: ¿dos entidades mutuamente relacionadas?
    (2019) Mendoza-Torres, Evelyn; Bravo-Sagua, Roberto; Villa, Mónica; Flores, Nancy; Olivares, María José; Calle, Ximena; Riquelme, Jaime A.; Bambs S., Claudia; Castro Gálvez, Pablo Federico; Lavandero, Sergio
    Las enfermedades cardiovasculares y el cáncer son enfermedades crónicas transmisibles culturalmente, y las dos causas principales de mortalidad en el mundo. Además del gran impacto sobre la mortalidad y morbilidad, estas enfermedades han mostrado un alto grado de relación entre ellas debido, entre otras razones, a que comparten factores de riesgo y mecanismos biológicos. La alta incidencia de enfermedad cardiovascular en pacientes con cáncer es un fenómeno conocido que ha orientado el desarrollo del campo interdisciplinario de la cardio-oncología. Sin embargo, en la última década han surgido evidencias que muestran el papel que desempeñan las enfermedades cardiovasculares en el desarrollo de cáncer. Un estudio reciente publicado por Meijers y cols, en agosto de 2018 en Circulation, mostró que la insuficiencia cardiaca post-infarto del miocardio contribuye significativamente al desarrollo del cáncer de colón, apoyando lo obtenido en estudios epidemiológicos anteriores. Este estudio también sugiere que el crecimiento tumoral podría producirse por factores secretados por el corazón insuficiente abriendo un amplio grupo de posibilidades de investigación en lo que sería un nuevo campo de la medicina cuyo propósito sería el desarrollo de nuevas estrategias para el seguimiento y tratamiento del cáncer en pacientes con enfermedades cardiovasculares. El presente artículo revisa los factores de riesgo, y mecanismos celulares y moleculares, que son comunes en las enfermedades cardiovasculares y el cáncer, la contribución del trabajo de Meijers y cols hacia un mayor entendimiento de la interrelación entre estas patologías y las perspectivas futuras con respecto a los nuevos hallazgos.
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    Light-induced release of the cardioprotective peptide angiotensin-(1-9) from thermosensitive liposomes with gold nanoclusters
    (2020) Bejarano, Julian; Rojas, Aldo; Ramirez Sagredo, Andrea; Riveros, Ana L.; Morales Zavala, Francisco; Flores, Yvo; Riquelme, Jaime A.; Guzman, Fanny; Araya, Eyleen; Chiong, Mario; Ocaranza, María Paz; Morales, Javier O.; Villamizar Sarmiento, Maria Gabriela; Sanchez, Gina; Lavandero, Sergio; Kogan, Marcelo J.
    Angiotensin-(1-9), a component of the non-canonical renin-angiotensin system, has a short half-life in blood. This peptide has shown to prevent and/or attenuate hypertension and cardiovascular remodeling. A controlled release of angiotensin-(1-9) is needed for its delivery to the heart. Our aim was to develop a drug delivery system for angiotensin-(1-9). Thermosensitive liposomes (LipoTherm) were prepared with gold nanoclusters (LipoThermAuNC) to increase the stability and reach a temporal and spatial control of angiotensin-(1-9) release. Encapsulation efficiencies of nearly 50% were achieved in LipoTherm, reaching a total angiotensin-(1-9) loading of around 180 mu M. This angiotensin-(1-9)-loaded LipoTherm sized around 100 nm and exhibited a phase transition temperature of 43.C. AuNC were grown on LipoTherm and the new hybrid nanosystem showed energy absorption in the near-infrared (NIR) wavelength range. By NIR laser irradiation, a controlled release of angiotensin-(1-9) was achieved from the LipoTherm-AuNC nanosystem. These nanosystems did not show any cytotoxic effect on cultured cardiomyocytes. Biological activity of angiotensin-(1-9) released from the LipoTherm-AuNCbased nanosystem was confirmed using an ex vivo Langendorff heart model.
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    New Molecular Insights of Insulin in Diabetic Cardiomyopathy
    (2016) Westermeier, Francisco; Riquelme, Jaime A.; Pavez, Mario; Garrido, Valeria; Diaz, Ariel; Verdejo Pinochet, Hugo; Castro Gálvez, Pablo Federico; Garcia, Lorena; Lavandero, Sergio
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    Protection of the myocardium against ischemia/reperfusion injury by angiotensin-(1–9) through an AT2R and Akt-dependent mechanism
    (2018) Mendoza Torres, Evelyn; Riquelme, Jaime A.; Vielma Zuñiga, Alejandra Loreto; Ramírez Sagredo, Andrea; Gabrielli, Luigi; Bravo Sagua, Roberto; Jalil Milad, Jorge; Rothermel, Beverly A.; Sánchez, Gina; Ocaranza, María Paz; Lavandero, Sergio
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    Regulation of total LC3 levels by angiotensin II in vascular smooth muscle cells
    (2022) Mondaca-Ruff, David; Quiroga, Clara; Norambuena-Soto, Ignacio; Riquelme, Jaime A.; San Martin, Alejandra; Bustamante, Mario; Lavandero, Sergio; Chiong, Mario
    Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we studied how Ang II regulates LC3 levels in VSMCs and whether Bag3, a co-chaperone known to regulate LC3 total levels, may be involved in the effects elicited by Ang II. A7r5 cell line or rat aortic smooth muscle cell (RASMC) primary culture were stimulated with Ang II 100 nM for 24 h and LC3 I, LC3 II and Bag3 protein levels were determined by Western blot. MAP1LC3B mRNA levels were assessed by RT-qPCR. Ang II increased MAP1LC3B mRNA levels and protein levels of LC3 I, LC3 II and total LC3 (LC3 I + LC3 II). Cycloheximide, but not actinomycin D, abolished LC3 II and total LC3 increase elicited by Ang II in RASMCs. In A7r5 cells, cycloheximide prevented the Ang II-mediated increase of LC3 I and total LC3, but not LC3 II. Moreover, Ang II increased Bag3 levels, but this increase was not observed upon co-administration with either losartan 1 mu M (AT1R antagonist) or Y-27632 10 mu M (ROCK inhibitor). These results suggest that Ang II may regulate total LC3 content through transcriptional and translational mechanisms. Moreover, Bag3 is increased in response to Ang II by a AT1R/ROCK signalling pathway. These data provide preliminary evidence suggesting that Ang II may stimulate autophagy in VSMCs by increasing total LC3 content and LC3 processing.