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Neurochem Res. 2017 Sep;42(9):2479-2489. doi: 10.1007/s11064-017-2343-4. Epub 2017 Jul 12.

The Role of the Oligodendrocyte Lineage in Acute Brain Trauma.

Author information

1
Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, 66421, Homburg, Germany.
2
Molecular Physiology, Center for Integrative Physiology and Molecular Medicine (CIPMM), University of Saarland, 66421, Homburg, Germany. frank.kirchhoff@uks.eu.

Abstract

An acute brain injury is commonly characterized by an extended cellular damage. The post-injury process of scar formation is largely determined by responses of various local glial cells and blood-derived immune cells. The role of astrocytes and microglia have been frequently reviewed in the traumatic sequelae. Here, we summarize the diverse contributions of oligodendrocytes (OLs) and their precursor cells (OPCs) in acute injuries. OLs at the lesion site are highly sensitive to a damaging insult, provoked by Ca2+ overload after hyperexcitation originating from increased levels of transmitters. At the lesion site, differentiating OPCs can replace injured oligodendrocytes to guarantee proper myelination that is instrumental for healthy brain function. In contrast to finally differentiated and non-dividing OLs, OPCs are the most proliferative cells of the brain and their proliferation rate even increases after injury. There exist even evidence that OPCs might also generate some type of astrocyte beside OLs. Thereby, OPCs can contribute to the generation and maintenance of the glial scar. In the future, detailed knowledge of the molecular cues that help to prevent injury-evoked glial cell death and that control differentiation and myelination of the oligodendroglial lineage will be pivotal in developing novel therapeutic approaches.

KEYWORDS:

Astrocytes; Myelination; NG2 glia; Oligodendrocyte precursor; Oligodendrocytes; Traumatic brain injury

PMID:
28702713
DOI:
10.1007/s11064-017-2343-4
[Indexed for MEDLINE]

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