MicroRNAs control the apoptotic threshold in primed pluripotent stem cells through regulation of BIM
| Autor: | Pernaute, B, Spruce, T, Smith, K M, Sanchez-Nieto, J M, Manzanares, M, Cobb, B S, Rodriguez, T A |
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| Přispěvatelé: | Fundación ProCNIC, Medical Research Council (Reino Unido), European Molecular Biology Organization, Unión Europea. Comisión Europea, Medical Research Council (MRC) |
| Rok vydání: | 2014 |
| Předmět: |
EXPRESSION
Pluripotency Pluripotent Stem Cells Cell Survival AUTOIMMUNITY Apoptosis DISEASE Research Communication Mice Proto-Oncogene Proteins Animals Bim DNA METHYLATION 11 Medical and Health Sciences Cells Cultured Genetics & Heredity Science & Technology MIRNA CLUSTERS Epiblast Bcl-2-Like Protein 11 epiblast Gene Expression Profiling MOUSE DEVELOPMENT Membrane Proteins Gene Expression Regulation Developmental Cell Biology LINEAGE 06 Biological Sciences pluripotency DICER FAMILY 17 Psychology and Cognitive Sciences microRNAs Mitochondria MicroRNAs DIFFERENTIATION Apoptosis Regulatory Proteins Life Sciences & Biomedicine Developmental Biology Dicer |
| Zdroj: | Repisalud Instituto de Salud Carlos III (ISCIII) Genes & Development |
| Popis: | Mammalian primed pluripotent stem cells have been shown to be highly susceptible to cell death stimuli due to their low apoptotic threshold, but how this threshold is regulated remains largely unknown. Here we identify microRNA (miRNA)-mediated regulation as a key mechanism controlling apoptosis in the post-implantation epiblast. Moreover, we found that three miRNA families, miR-20, miR-92, and miR-302, control the mitochondrial apoptotic machinery by fine-tuning the levels of expression of the proapoptotic protein BIM. These families therefore represent an essential buffer needed to maintain cell survival in stem cells that are primed for not only differentiation but also cell death. M.M. was supported by the Spanish Government and the ProCNIC Foundation. This work was supported by the Medical Research Council (MR/K00090X/1), EMBO (ALTF 1340-2010), and the European Commission (PIEF-GA-2010-273884 - MEMD). Sí |
| Databáze: | OpenAIRE |
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