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Event Abstract Back to Event Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence Sonia L. Albarracin1*, Bernd R. Stab1*, Maria C. Tovar1, Laura Martinez1 and Mabel A. Grismaldo1 1 Pontificia Universidad Javeriana, Nutrition and Biochemistry, Colombia Astrocytes are highly specialized cells that can maintain the integrity of the synapse, facilitate nutrition and trophic support to neurons, and regulate metabolic coupling between neurons and glia. However, astrocytes are involved in resolving different types of injuries and in aging processes in the brain. Senescence has also been reported in the brain, and senescence-associated loss of astrocyte function is linked to neuronal dysfunction in age-related neurodegenerative diseases such as Alzheimer’s disease and Parkinson's disease. For example, astrocyte senescence per se inhibits synapse maturation and affects synaptic transmission. In response to the cell’s bio-energetic state, mitochondria continuously undergo structural remodeling through fission and fusion processes. These tightly regulated events are believed to be involved in many cellular events such as apoptosis, senescence, and age-related diseases. Although, little is known about the age-related changes that occur in astrocytes and if these cells are able to generate a senescent phenotype mediated by mitochondria, in the present study we evaluated the involvement of mitochondrial remodeling in the senescence process of rat astrocytes in vitro. The results obtained showed that when comparing cells at population doubling two (PD2) with cells at population doubling ten (PD10) there is a significant increase in the activity of the senescence-associated β-galactosidase marker in PD10 cells. In addition, PD10 cells had increased mitochondrial volume, decreased superoxide production, and decreased mitochondrial membrane potential. Protein characterization evidenced changes in the balance between mitochondrial fission and fusion proteins. Collectively, our results demonstrated a senescent-astrocyte phenotype at PD10, which is associated with metabolic and mitochondrial phenotype changes. Acknowledgements This work was supported by grants Pontificia Universidad Javeriana ID 4468. References Andreyev, A.Y., Y.E. Kushnareva, and Starkov, A.A. (2005). Mitochondrial metabolism of reactive oxygen species. Biochemistry (Mosc). 70, 200-214. Griffin, E.E., S.A. Detmer, and Chan, D.C. (2006). Molecular mechanism of mitochondrial membrane fusion. Biochim Biophys Acta, 1763, 482-489. Hoppins, S., Lackner, L. and Nunnari, J. (2007). The machines that divide and fuse mitochondria. Annu Rev Biochem, 2007. 76, 751-780. Sanz, A. and Stefanatos, R.K. (2008). The mitochondrial free radical theory of aging: a critical view. Curr Aging Sci, 1, 10-21. Ziegler, D.V., Wiley, C.D., and Velarde, M.C. (2015). Mitochondrial effectors of cellular senescence: beyond the free radical theory of aging. Aging Cell, 14, 1-7. doi: 10.1111/acel.12287 Keywords: Aging, Astrocytes, Mitochondria, Reactive Oxygen Species, senescence, mitochondrial fission and fusion proteins, neurodegeneration Conference: Latin-American School on glial cells in the diseased brain (IBRO), Bogotá, Colombia, 13 Jul - 17 Jul, 2015. Presentation Type: Poster Presentation Topic: Neural excitability, synaptic transmission, glia: Cellular and molecular mechanisms Citation: Albarracin SL, Stab BR, Tovar MC, Martinez L and Grismaldo MA (2015). Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence. Conference Abstract: Latin-American School on glial cells in the diseased brain (IBRO). doi: 10.3389/conf.fncel.2015.35.00030 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 23 Feb 2015; Published Online: 11 Jun 2015. * Correspondence: Dr. Sonia L Albarracin, Pontificia Universidad Javeriana, Nutrition and Biochemistry, Bogota, D.C., Colombia, albarra@javeriana.edu.co Dr. Bernd R Stab, Pontificia Universidad Javeriana, Nutrition and Biochemistry, Bogota, D.C., Colombia, b.r.stab@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Sonia L Albarracin Bernd R Stab Maria C Tovar Laura Martinez Mabel A Grismaldo Google Sonia L Albarracin Bernd R Stab Maria C Tovar Laura Martinez Mabel A Grismaldo Google Scholar Sonia L Albarracin Bernd R Stab Maria C Tovar Laura Martinez Mabel A Grismaldo PubMed Sonia L Albarracin Bernd R Stab Maria C Tovar Laura Martinez Mabel A Grismaldo Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. 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