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

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.

Enterococcus faecalis attenuates osteogenesis through activation of p38 and ERK1/2 pathways in MC3T3‐E1 cells

“…), 5′‐ TGGTGATGAAGGGGTCATTTATG‐3′ and 5′‐TTCGGCTTTCCAGTCAGACTC‐3′ forward and reverse primers for Caspase‐3 (Jones et al . ) and 5′‐ATGTGTCCGTCGTGGATCTGA‐3′ and 5′‐ATGCCTGCTTCACCACCTTCT‐3′ forward and reverse primers for GAPDH (Fratini et al . ).…”

A novel approach of human embryonic stem cells therapy in treatment of Friedrich's Ataxia

“…In FA, the mechanism to remove the reactive oxygen species (ROS) is impaired leading to oxidative stress and cell death [7,9]. Stem cells may have ability to protect cells susceptible to oxidative stress that occurs in many neurodegenerative diseases like FRDA [9].…”

“…The transcription of certain oxidative stress-related genes was also activated. Thus, autologous stem cells transplantation in FRDA patients may protect the affected neurons [9]. Stem cells such as mesenchymal stem cell, ESCs, induced pluripotent stem cells are capable of producing trophic factors [22].…”

“…But there is no proof of the positive results in the neurological aspects of the disorder. Thus, alternative approaches must be developed to treat FRDA [9]. Human embryonic stem cells (hESCs) have unlimited proliferative capacity and potential to differentiate into all types of somatic cells [10,11].…”

“…Human embryonic stem cells (hESCs) have unlimited proliferative capacity and potential to differentiate into all types of somatic cells [10,11]. According to Jones et al, if stem cells are transplanted near the affected cells that are under oxidative stress, they can produce tropic factors, thereby increasing the survival of the cells in FRDA patients [9].…”