Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence

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 t...

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Main Author: Sonia Luz Albarracin
Format: Article
Language:English
Published: Frontiers Media S.A. 2015-02-01
Series:Frontiers in Cellular Neuroscience
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/conf.fncel.2015.35.00030/full
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author Sonia Luz Albarracin
author_facet Sonia Luz Albarracin
author_sort Sonia Luz Albarracin
collection DOAJ
description 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.
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spelling doaj.art-3dd464d7b3ce4024bce4b4cefa3bef6b2022-12-22T02:19:09ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022015-02-01910.3389/conf.fncel.2015.35.00030139528Mitochondrial fission and fusion in astrocytes: a new pathway towards senescenceSonia Luz Albarracin0Pontificia Universidad JaverianaAstrocytes 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.http://journal.frontiersin.org/Journal/10.3389/conf.fncel.2015.35.00030/fullAgingAstrocytesMitochondriaReactive Oxygen Speciessenescenceneurodegenerationmitochondrial fission and fusion proteins
spellingShingle Sonia Luz Albarracin
Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence
Frontiers in Cellular Neuroscience
Aging
Astrocytes
Mitochondria
Reactive Oxygen Species
senescence
neurodegeneration
mitochondrial fission and fusion proteins
title Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence
title_full Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence
title_fullStr Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence
title_full_unstemmed Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence
title_short Mitochondrial fission and fusion in astrocytes: a new pathway towards senescence
title_sort mitochondrial fission and fusion in astrocytes a new pathway towards senescence
topic Aging
Astrocytes
Mitochondria
Reactive Oxygen Species
senescence
neurodegeneration
mitochondrial fission and fusion proteins
url http://journal.frontiersin.org/Journal/10.3389/conf.fncel.2015.35.00030/full
work_keys_str_mv AT sonialuzalbarracin mitochondrialfissionandfusioninastrocytesanewpathwaytowardssenescence