Ciencias Exactas y Ciencias de la Salud
Permanent URI for this collectionhttps://hdl.handle.net/11285/551039
Pertenecen a esta colección Tesis y Trabajos de grado de las Maestrías correspondientes a las Escuelas de Ingeniería y Ciencias así como a Medicina y Ciencias de la Salud.
Browse
Search Results
- Effect of estradiol on Ca2+ handling proteins in hypertrophied H9c2-derived myotubes(Instituto Tecnológico y de Estudios Superiores de Monterrey, 2021-05-31) López Morán, Silvia Araceli; ALTAMIRANO BARRERA, JULIO; 245746; Altamirano Barrera, Julio; puelquio/mscuervo; De la Garza Hernández, Ana Laura Isabel; Gómez Viquez, Norma Leticia; García Varela, Rebeca; Escuela de Ingeniería y Ciencias; Campus Monterrey; García Rivas, Gerardo de JesúsCardiac hypertrophy is characterized by abnormal growth of muscle mass, accompanied by dysregulations in cell structure and function, and can lead to heart failure. Some of the main changes that hypertrophic cells undergo are sarcomere disorganization, loss of T tubules, alterations in Ca2+ management, and cardiac contractility. There is a higher prevalence of cardiovascular diseases in young and middle-aged men compared to women, which is why female sex hormones (being 17β-Estradiol the main circulating female sex hormone) are considered to play a cardioprotective role. Cardiac hypertrophy, its molecular mechanisms and therapeutic strategies have traditionally been studied in different in vivo and in vitro models. Each model has advantages and disadvantages, such as challenging maintenance in primary cells or lack of complete cardiac phenotype in immortalized cell lines. The H9c2 cell line can be differentiated into myotubes, using retinoic acid as the inducing agent, to have a phenotype more cardiac-like. In this project it was standardized a model of hypertrophied H9c2-derived myotubes induced by angiotensin II, and the model was used to assess the cardioprotective role of pretreatment with 17β-Estradiol in terms of inflammation markers, gene expression of Ca2+ regulatory proteins, assessed by qPCR, and cell hypertrophy assessed by confocal microscopy. It was observed an attenuation of hypertrophic phenotype in differentiated myotubes with 17β-Estradiol pretreatment.
- The role of the mitochondrial calcium uniporter in the process of arrhythmogenesis in a murine model of acute catecholamine overload(Instituto Tecnológico y de Estudios Superiores de Monterrey, 2020-05-22) Salazar Ramírez, Felipe de Jesús; SALAZAR RAMIREZ, FELIPE DE JESUS; 876167; García Rivas, Gerardo de Jesús; emipsanchez; Alves Figueiredo, Hugo Jorge; Rojas Martínez, Augusto; Ramos Mondragón, Roberto; Escuela de Medicina y Ciencias de la Salud; Campus MonterreySudden cardiac death by fulminant ventricular arrhythmias remains a concern in population with cardiac risk. Recently, the mitochondrion has been implied to be a central player in Ca2+ mishandling, with its dysfunction leading up to arrhythmogenesis. A possible starting event that could lead to most changes seen in cardiac disfunction is mitochondrial Ca2+ overload. The following research study focuses on demonstrating the effects of mitochondrial Ca2+ influx inhibition in arrhythmogenesis. A murine model of acute catecholamine (isoproterenol) overload was treated previously with mitochondrial Ca2+ transport inhibitor Ru360. Ru360 treated mice showed a complete abolishment of ventricular tachycardia and ventricular fibrillation. To characterize the possible mechanisms of action, heart mitochondria were isolated and mitochondrial function was assessed. Mitochondrial Ca2+ transport inhibition preserved mitochondrial function and membrane integrity as demonstrated by a higher respiratory control and calcium retention capacity when compared to isoproterenol-treated mice which appears to be caused by a reduced oxidative stress as a trend to preserve reduced thiol groups was shown. Given the positive results obtained in abolishing ventricular arrhythmias by inhibiting mitochondrial Ca2+ transport, it is precise to continue the characterization of the mechanisms by which this therapy exerts its effects. To fully demonstrate its efficacy and characterize its mechanism of action may lead up to a new therapeutic target and therapy that could set the bases to clinical research in the near future.