Startseite Could the inhibitor of DNA binding 2 and 4 play a role in white matter injury?
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Could the inhibitor of DNA binding 2 and 4 play a role in white matter injury?

  • Xiaoyun Gou , Ying Tang , Yi Qu , Dongqiong Xiao , Junjie Ying und Dezhi Mu EMAIL logo
Veröffentlicht/Copyright: 9. Februar 2019
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Abstract

White matter injury (WMI) prevents the normal development of myelination, leading to central nervous system myelination disorders and the production of chronic sequelae associated with WMI, such as chronic dyskinesia, cognitive impairment and cerebral palsy. This results in a large emotional and socioeconomic burden. Decreased myelination in preterm infant WMI is associated with the delayed development or destruction of oligodendrocyte (OL) lineage cells, particularly oligodendrocyte precursor cells (OPCs). The development of cells from the OL lineage involves the migration, proliferation and different stages of OL differentiation, finally leading to myelination. A series of complex intrinsic, extrinsic and epigenetic factors regulate the OPC cell cycle withdrawal, OL lineage progression and myelination. We focus on the inhibitor of DNA binding 2 (ID2), because it is widely involved in the different stages of OL differentiation and genesis. ID2 is a key transcription factor for the normal development of OL lineage cells, and the pathogenesis of WMI is closely linked with OL developmental disorders. ID4, another family member of the IDs protein, also plays a similar role in OL differentiation and genesis. ID2 and ID4 belong to the helix-loop-helix family; they lack the DNA-binding sequences and inhibit oligodendrogenesis and OPC differentiation. In this review, we mainly discuss the roles of ID2 in OL development, especially during OPC differentiation, and summarize the ID2-mediated intracellular and extracellular signaling pathways that regulate these processes. We also discuss ID4 in relation to bone morphogenetic protein signaling and oligodendrogenesis. It is likely that these developmental mechanisms are also involved in the myelin repair or remyelination in human neurological diseases.

Award Identifier / Grant number: 81330016

Award Identifier / Grant number: 81630038

Award Identifier / Grant number: 81771634

Award Identifier / Grant number: 2017YFA0104200

Award Identifier / Grant number: IRT0935

Award Identifier / Grant number: 2016TD0002

Award Identifier / Grant number: 1311200003303

Funding statement: This work was supported by the National Science Foundation of China (Nos. 81330016, 81630038 and 81771634), the National Key Research and Development Program of China (No. 2017YFA0104200), the Ministry of Education of China (No. IRT0935), the Science and Technology Bureau of Sichuan Province (No. 2016TD0002) and by a grant of the clinical discipline program (Neonatology) from the Ministry of Health of China (1311200003303).

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Received: 2018-09-07
Accepted: 2018-11-02
Published Online: 2019-02-09
Published in Print: 2019-07-26

©2019 Walter de Gruyter GmbH, Berlin/Boston

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