Efecto de la senescencia sobre la dinámica mitocondrial en fibroblastos de embrión humano (WI-38)
Aging is a universal an irreversible physiological process that is related to continued deterioration as well as to the progressive loss of the organism's adaptive capacity. Senescence is a cellular phenomenon related to aging, which occurs when the cells reach their maximum replicative capacit...
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| Tipo de recurso: | tesis de maestría |
| Estado: | Versión publicada |
| Fecha de publicación: | 2015 |
| País: | México |
| Institución: | Universidad Autónoma Metropolitana |
| Repositorio: | Repositorio Institucional de la UAM Iztapalapa |
| Idioma: | español |
| OAI Identifier: | oai:bindani.izt.uam.mx:n870zr298 |
| Acceso en línea: | https://doi.org/10.24275/uami.n870zr298 |
| Access Level: | acceso abierto |
| Palabra clave: | info:eu-repo/classification/LEM/Cells -- Aging info:eu-repo/classification/LEM/Mitocondria info:eu-repo/classification/LEM/Células -- Envejecimiento info:eu-repo/classification/LEM/Mitochondria info:eu-repo/classification/cti/3 |
| Sumario: | Aging is a universal an irreversible physiological process that is related to continued deterioration as well as to the progressive loss of the organism's adaptive capacity. Senescence is a cellular phenomenon related to aging, which occurs when the cells reach their maximum replicative capacity and therefore irreversibly stop the cell cycle in G1 phase. Cells can achieve senescence by different pathways or stimulus, such as telomere shortening during cellular proliferation, in which case the event is called replicative senescence (RS), or due to biomolecules' oxidative damage, and which is then called stress induced premature senescence (SIPS). It is now known that mitochondria are dynamic organelles able to modify their morphology due to subcellular processes such as mitochondrial fusion, fission, biogenesis, mitophagy and transport, which altogether are called mitochondrial dynamics (MD). During senescence cellular homeostasis changes, however the exact modifications in MD are still unclear and nothing is known about the differences in MD among diverse forms of senesce. Hence the aim of this work was to understand if there are variations in MD due to the pathway of senescence induction. Human lung fibroblasts WI38 were used to study MD in RS and SIPS. Some of MD's main effector proteins were determined by western blot: Opa1 (fusion), Drp1 (fission) and PGC1 (biogenesis). Our results showed that Opa1 decreased during SIPS while Drp1 increased in SR. The mitochondrial network was also evaluated by confocal microscopy. Interestingly, SR cells maintained the normal tubular morphology, whereas SIPS cells presented hiperfused morphology in the center around the nucleus and at the same time fragmentation in the more remote zones. More experiments are necessary in order to completely characterize MD, however this work shows for the first time that MD in senescent cells might be different depending of the senescence induction path. |
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