Histone deacetylase inhibition is cytotoxic to oligodendrocyte precursor cells in vitro and in vivo

2016 ◽  
Vol 54 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Toros A. Dincman ◽  
Jason E. Beare ◽  
Sujata Saraswat Ohri ◽  
Vittorio Gallo ◽  
Michal Hetman ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Histone Deacetylase Inhibition ◽  
Oligodendrocyte Precursor

Immunology of oligodendrocyte precursor cells in vivo and in vitro

2019 ◽  
Vol 331 ◽  
pp. 28-35 ◽  
Author(s):  
Jack P. Antel ◽  
Yun Hsuan Lin ◽  
Qiao-Ling Cui ◽  
Florian Pernin ◽  
Timothy E. Kennedy ◽  
...  
Keyword(s):  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor

Inhibition of oligodendrocyte precursor motility by oligodendrocyte processes: implications for transplantation-based approaches to multiple sclerosis

1997 ◽  
Vol 3 (2) ◽  
pp. 162-167 ◽  
Author(s):  
Samantha Jefferson ◽  
Thomas Jacques ◽  
BW Kiernan ◽  
Suzanna Scott-Drew ◽  
Richard Milner ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
White Matter ◽  
Time Lapse ◽  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor ◽  
Normal White Matter ◽  
Successful Repair

Transplantation of oligodendrocyte precursor cells represents a promising approach to the treatment of the chronic demyelinated lesions of multiple sclerosis. In view of the multi-focal nature of the disease it will be necessary for the transplanted oligodendrocyte precursor cells to migrate through normal white matter between lesions. Work in other systems has shown that differentiated oligodendrocytes within white matter express molecules inhibitory for axon outgrowth. In light of this we have examined the effect of oligodendrocytes on the migration of oligodendrocyte precursors in vitro using time lapse video microscopy. We find that oligodendrocytes induce collapse and loss of motility in oligodendrocyte precursor processes, with this effect being lost as oligodendrocytes undergo programmed cell death. We conclude that the inhibitory factors present on differentiated oligodendrocytes may prevent effective migration between lesion in vivo, and that strategies to overcome this inhibition may be required for successful repair.

Analysis of motile oligodendrocyte precursor cells in vitro and in brain slices

Glia ◽  
1997 ◽  
Vol 20 (4) ◽  
pp. 284-298 ◽  
Author(s):  
Carolin Schmidt ◽  
Carsten Ohlemeyer ◽  
Charalampos Labrakakis ◽  
Tilmann Walter ◽  
Helmut Kettenmann ◽  
...  
Keyword(s):  
Brain Slices ◽  
Precursor Cells ◽  
Oligodendrocyte Precursor Cells ◽  
Oligodendrocyte Precursor

scholarly journals Deficiency of Mitochondrial Aspartate-Glutamate Carrier 1 Leads to Oligodendrocyte Precursor Cell Proliferation Defects Both In Vitro and In Vivo

2019 ◽  
Vol 20 (18) ◽  
pp. 4486 ◽  
Author(s):  
Sabrina Petralla ◽  
Luis Emiliano Peña-Altamira ◽  
Eleonora Poeta ◽  
Francesca Massenzio ◽  
Marco Virgili ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Cell Model ◽  
Precursor Cells ◽  
Trophic Factors ◽  
Psychomotor Development ◽  
Oligodendrocyte Precursor ◽  
Aspartate Glutamate Carrier

Aspartate-Glutamate Carrier 1 (AGC1) deficiency is a rare neurological disease caused by mutations in the solute carrier family 25, member 12 (SLC25A12) gene, encoding for the mitochondrial aspartate-glutamate carrier isoform 1 (AGC1), a component of the malate–aspartate NADH shuttle (MAS), expressed in excitable tissues only. AGC1 deficiency patients are children showing severe hypotonia, arrested psychomotor development, seizures and global hypomyelination. While the effect of AGC1 deficiency in neurons and neuronal function has been deeply studied, little is known about oligodendrocytes and their precursors, the brain cells involved in myelination. Here we studied the effect of AGC1 down-regulation on oligodendrocyte precursor cells (OPCs), using both in vitro and in vivo mouse disease models. In the cell model, we showed that a reduced expression of AGC1 induces a deficit of OPC proliferation leading to their spontaneous and precocious differentiation into oligodendrocytes. Interestingly, this effect seems to be related to a dysregulation in the expression of trophic factors and receptors involved in OPC proliferation/differentiation, such as Platelet-Derived Growth Factor α (PDGFα) and Transforming Growth Factor βs (TGFβs). We also confirmed the OPC reduction in vivo in AGC1-deficent mice, as well as a proliferation deficit in neurospheres from the Subventricular Zone (SVZ) of these animals, thus indicating that AGC1 reduction could affect the proliferation of different brain precursor cells. These data clearly show that AGC1 impairment alters myelination not only by acting on N-acetyl-aspartate production in neurons but also on OPC proliferation and suggest new potential therapeutic targets for the treatment of AGC1 deficiency.

Sign in / Sign up

Export Citation Format

Share Document