In:
Journal of Neurochemistry, Wiley, Vol. 127, No. 3 ( 2013-11), p. 426-433
Abstract:
Developing oligodendrocytes, collectively termed ‘pre‐myelinating oligodendrocytes’ (pre OL s), are vulnerable to hypoxic or ischemic insults. The underlying mechanism of this vulnerability remains unclear. Previously, we showed that Bcl‐2⁄E1B‐19K‐interacting protein 3 ( BNIP 3), a proapoptotic member of the Bcl‐2 family proteins, induced neuronal death in a caspase‐independent manner in stroke. In this study, we investigated the role of BNIP 3 in pre OL cell death induced by hypoxia or ischemia. In primary oligodendrocyte progenitor cell ( OPC ) cultures exposed to oxygen–glucose deprivation, we found that BNIP 3 was upregulated and levels of BNIP 3 expression correlated with the death of OPC s. Up‐regulation of BNIP 3 was observed in pre OL s in the white matter in a neonatal rat model of stroke. Knockout of BNIP 3 significantly reduced death of pre OL s in the middle cerebral artery occlusion model in mice. Our results demonstrate a role of BNIP 3 in mediating pre OL s cell death induced by hypoxia or ischemia, and suggest that BNIP 3 may be a new target for protecting oligodendrocytes from death after stroke. image Pre‐myelinating oligodendrocytes (preOLs) are known to be highly vulnerable to ischemic insults. It remains unclear, however, how preOLs die. This study shows that BNIP3, a proapoptotic member of the Bcl‐2 family proteins, is a mediator of hypoxia/ischemia‐induced preOLs death. The BNIP3 cell death pathway may therefore be a new target for protecting oligodendrocytes from death after stroke.
Type of Medium:
Online Resource
ISSN:
0022-3042
,
1471-4159
DOI:
10.1111/jnc.2013.127.issue-3
Language:
English
Publisher:
Wiley
Publication Date:
2013
detail.hit.zdb_id:
2020528-4
SSG:
12
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