Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells

Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells

Many neurodegenerative disorders share a common susceptibility to oxidative stress, including Alzheimer’s, Parkinson Disease, Huntington Disease and Friedreich’s ataxia. In a previous work, we proved that stem cell-conditioned medium increased the survival of cells isolated from Friedreich’s ataxia...

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Main Authors: Jones, Jonathan, Estirado, Alicia, Redondo, Carolina, Martinez, Salvador
Format: Online
Language:English
Published: Public Library of Science 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650052/
id pubmed-3650052
recordtype oai_dc
spelling pubmed-36500522013-05-13 Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells Jones, Jonathan Estirado, Alicia Redondo, Carolina Martinez, Salvador Research Article Many neurodegenerative disorders share a common susceptibility to oxidative stress, including Alzheimer’s, Parkinson Disease, Huntington Disease and Friedreich’s ataxia. In a previous work, we proved that stem cell-conditioned medium increased the survival of cells isolated from Friedreich’s ataxia patients, when submitted to oxidative stress. The aim of the present work is to confirm this same effect in dorsal root ganglia cells isolated from YG8 mice, a mouse model of Friedreich’s ataxia. In this disorder, the neurons of the dorsal root ganglia are the first to degenerate. Also, in this work we cultured mesenchymal stem cells isolated from YG8 mice, in order to compare them with their wildtype counterpart. To this end, dorsal root ganglia primary cultures isolated from YG8 mice were exposed to oxidative stress and cultured with conditioned medium from either wildtype or YG8 stem cells. As a result, the conditioned medium increased the survival of the dorsal root ganglia cells. This coincided with an increase in oxidative stress-related markers and frataxin expression levels. BDNF, NT3 and NT4 trophic factors were detected in the conditioned medium of both wild-type and YG8 stem cells, all which bind to the various neuronal cell types present in the dorsal root ganglia. No differences were observed in the stem cells isolated from wildtype and YG8 mice. The results presented confirm the possibility that autologous stem cell transplantation may be a viable therapeutic approach in protecting dorsal root ganglia neurons of Friedreich’s ataxia patients. Public Library of Science 2013-05-09 /pmc/articles/PMC3650052/ /pubmed/23671637 http://dx.doi.org/10.1371/journal.pone.0062807 Text en © 2013 Jones et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Jones, Jonathan
Estirado, Alicia
Redondo, Carolina
Martinez, Salvador
spellingShingle Jones, Jonathan
Estirado, Alicia
Redondo, Carolina
Martinez, Salvador
Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells
author_facet Jones, Jonathan
Estirado, Alicia
Redondo, Carolina
Martinez, Salvador
author_sort Jones, Jonathan
title Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells
title_short Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells
title_full Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells
title_fullStr Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells
title_full_unstemmed Stem Cells from Wildtype and Friedreich’s Ataxia Mice Present Similar Neuroprotective Properties in Dorsal Root Ganglia Cells
title_sort stem cells from wildtype and friedreich’s ataxia mice present similar neuroprotective properties in dorsal root ganglia cells
description Many neurodegenerative disorders share a common susceptibility to oxidative stress, including Alzheimer’s, Parkinson Disease, Huntington Disease and Friedreich’s ataxia. In a previous work, we proved that stem cell-conditioned medium increased the survival of cells isolated from Friedreich’s ataxia patients, when submitted to oxidative stress. The aim of the present work is to confirm this same effect in dorsal root ganglia cells isolated from YG8 mice, a mouse model of Friedreich’s ataxia. In this disorder, the neurons of the dorsal root ganglia are the first to degenerate. Also, in this work we cultured mesenchymal stem cells isolated from YG8 mice, in order to compare them with their wildtype counterpart. To this end, dorsal root ganglia primary cultures isolated from YG8 mice were exposed to oxidative stress and cultured with conditioned medium from either wildtype or YG8 stem cells. As a result, the conditioned medium increased the survival of the dorsal root ganglia cells. This coincided with an increase in oxidative stress-related markers and frataxin expression levels. BDNF, NT3 and NT4 trophic factors were detected in the conditioned medium of both wild-type and YG8 stem cells, all which bind to the various neuronal cell types present in the dorsal root ganglia. No differences were observed in the stem cells isolated from wildtype and YG8 mice. The results presented confirm the possibility that autologous stem cell transplantation may be a viable therapeutic approach in protecting dorsal root ganglia neurons of Friedreich’s ataxia patients.
publisher Public Library of Science
publishDate 2013
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650052/
_version_ 1611976740471570432

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