Abstract
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.
Highlights
The term oxidative stress is used when there is an imbalance in the cell of reactive oxygen species and the molecules responsible for the removal of these elements
Dorsal root ganglia cells isolated from YG8 mice were cultured under different conditions: 1) standard culture medium (DMEM plus FBS and penicillin/streptomycin), 2) exposed to H2O2, and H2O2 with conditioned medium isolated from mesenchymal stem cells of wildtype (MSC-WT, 3) or YG8 mice (MSC-AtF, 4) (Figure 1 A–D, respectively)
We demonstrated that bone marrow mesenchymal stem cells from a Friedreich’s ataxia (FA) mouse model, presented similar neurotrophic properties than their wild-type counterpart
Summary
The term oxidative stress is used when there is an imbalance in the cell of reactive oxygen species and the molecules responsible for the removal of these elements. The increased frequency of this condition is known to be related to aging [1], there are certain diseases where the patients are more susceptible to this condition These include Alzheimer’s disease, Parkinson, multiple sclerosis, multiple system atrophy, progressive supranuclear atrophy, and Huntington’s disease [2]. Despite their different etiology, these disorders share this common trait in which mitochondrial dysfunction is strongly related [3]. Iron accumulation due to mitochondrial dysfunction or iron metabolism dysregulation is common in these disorders, which is toxic and causes cell death [4] Another disease where oxidative stress plays a major role is Friedreich’s ataxia (FA). For a review on oxidative stress and its role in FA see [10]
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