Generation of Oligodendrocytes from Human Pluripotent and Embryonic Stem Cells

Mattingly, Zoe A.; Chetty, Sundari

doi:10.1007/978-1-0716-3287-1_8

Cited by 2 publications

(1 citation statement)

References 19 publications

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“…Most recently a variation on the Douvaras and Fossati (2015) protocol showed that supplementation of media with the promyelinating compound clemastine fumarate reduced the differentiation time of OPCs to OLs down to 28 days ( Assetta et al, 2020 ; Mattingly and Chetty, 2023 ). Clemastine was previously identified as a promyelinating compound independent from its use as an antihistamine ( Li et al, 2015 ; Liu et al, 2016 ; Green et al, 2017 ; Bohlen et al, 2023 ) and its ability to promote OPC differentiation appears to be through blockade of the M1 muscarinic acetylcholine receptor, which is a most common subtype of muscarinic acetylcholine receptor which regulates OPC proliferation and differentiations ( Xiang et al, 2012 ; Chen et al, 2021 ; Palma et al, 2022 ).…”

Section: Hipsc Derived Oligodendrocyte Brain Modelsmentioning

confidence: 99%

Utilizing hiPSC-derived oligodendrocytes to study myelin pathophysiology in neuropsychiatric and neurodegenerative disorders.

Shim,

Romero-Morales,

Sripathy

et al. 2024

Front. Cell. Neurosci.

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Oligodendrocytes play a crucial role in our central nervous system (CNS) by myelinating axons for faster action potential conduction, protecting axons from degeneration, structuring the position of ion channels, and providing nutrients to neurons. Oligodendrocyte dysfunction and/or dysmyelination can contribute to a range of neurodegenerative diseases and neuropsychiatric disorders such as Multiple Sclerosis (MS), Leukodystrophy (LD), Schizophrenia (SCZ), and Autism Spectrum Disorder (ASD). Common characteristics identified across these disorders were either an inability of oligodendrocytes to remyelinate after degeneration or defects in oligodendrocyte development and maturation. Unfortunately, the causal mechanisms of oligodendrocyte dysfunction are still uncertain, and therapeutic targets remain elusive. Many studies rely on the use of animal models to identify the molecular and cellular mechanisms behind these disorders, however, such studies face species-specific challenges and therefore lack translatability. The use of human induced pluripotent stem cells (hiPSCs) to model neurological diseases is becoming a powerful new tool, improving our understanding of pathophysiology and capacity to explore therapeutic targets. Here, we focus on the application of hiPSC-derived oligodendrocyte model systems to model disorders caused by oligodendrocyte dysregulation.

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