<scp>BNIP</scp>3 mediates pre‐myelinating oligodendrocyte cell death in hypoxia and ischemia

Li, Chengren; Guan, Teng; Chen, Xueping; Li, Wenyan; Cai, Qian; Niu, Jianqin; Xiao, Lan; Kong, Jiming

doi:10.1111/jnc.12314

Cited by 28 publications

(26 citation statements)

References 26 publications

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“…Knockout of BNIP3 significantly reduced death of OPCs in the MCAO mouse model. This study provided further evidence of the molecular pathway underlying NG2‐glia cell death in ischemia . Furthermore, when Lee et al.…”

Section: Excitotoxicity Induced Ng2‐glia Cell Death In Ischemiasupporting

confidence: 62%

Roles of NG2‐glia in ischemic stroke

et al. 2017

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Recent studies have shown that a widely distributed class of glial cells, termed NG2-glia, engages in rapid signaling with surrounding neurons through direct synaptic contacts in the developing and mature central nervous system (CNS). This unique glial cell group has a typical function of proliferating and differentiating into oligodendrocytes during early development of the brain, which is crucial to axon myelin formation. Therefore, NG2-glia are also called oligodendrocyte precursor cells (OPCs). In vitro and in vivo studies reveal that NG2-glia expressing receptors and ion channels demonstrate functional significance for rapid signaling with neuronal synapses and modulation of neuronal activities in both physiological and pathological conditions. Although it is well known that NG2-glia play an important role in demyelinating diseases such as multiple sclerosis, little is known about how NG2-glia or OPCs impact neurons and brain function following ischemic injury. This review summarizes recent progress on the roles of NG2-glia in ischemic stroke and illustrates new approaches for targeting NG2-glia in the brain to treat this disease.

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Section: Excitotoxicity Induced Ng2‐glia Cell Death In Ischemiasupporting

confidence: 62%

Roles of NG2‐glia in ischemic stroke

et al. 2017

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“…Transient focal cerebral ischemia was induced using an intraluminal filament model of middle cerebral artery occlusion (MCAO), as previously described . Briefly, mice were anesthetized with isoflurane (1.5%‐2%), and rectal temperature was maintained at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…Protein lysates were prepared, and Western blotting (WB) was performed using our standard protocols . Samples were loaded on 10% SDS polyacrylamide gel and then transferred to a polyvinylidene difluoride membrane.…”

Section: Methodsmentioning

confidence: 99%

“…Transient focal cerebral ischemia was induced using an intraluminal filament model of middle cerebral artery occlusion (MCAO), as previously described. 5 Briefly, mice were anesthetized with isoflurane (1.5%-2%), and rectal temperature was maintained at 37°C. A 6-0 silicone-coated nylon monofilament (Doccol, Sharon, MA, USA) was inserted via the right external carotid artery until it obstructed the MCA, and the common carotid artery was simultaneously ligated for the duration of the ischemic period.…”

Section: Middle Cerebral Artery Occlusionmentioning

confidence: 99%

“…Protein lysates were prepared, and Western blotting (WB) was performed using our standard protocols. 5 Samples were loaded on 10% SDS polyacrylamide gel and then transferred to a polyvinylidene difluoride membrane. Membranes were blocked with 5% (w/v) milk in TBS buffer containing 0.05% Tween-20 for 1 hour and then incubated with specifying primary antibodies overnight at room temperature.…”

Section: Western Blottingmentioning

confidence: 99%

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Monocarboxylate transporter 1 and the vulnerability of oligodendrocyte lineage cells to metabolic stresses

et al. 2017

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HIF-1α/Beclin1-Mediated Autophagy Is Involved in Neuroprotection Induced by Hypoxic Preconditioning

Tan

et al. 2018

J Mol Neurosci

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Hypoxic preconditioning (HPC) exerts a protective effect against hypoxic/ischemic brain injury, and one mechanism explaining this effect may involve the upregulation of hypoxia-inducible factor-1 (HIF-1). Autophagy, an endogenous protective mechanism against hypoxic/ischemic injury, is correlated with the activation of the HIF-1α/Beclin1 signaling pathway. Based on previous studies, we hypothesize that the protective role of HPC may involve autophagy occurring via activation of the HIF-1α/Beclin1 signaling pathway. To test this hypothesis, we evaluated the effects of HPC on oxygen-glucose deprivation/reperfusion (OGD/R)-induced apoptosis and autophagy in SH-SY5Y cells. HPC significantly attenuated OGD/R-induced apoptosis, and this effect was suppressed by the autophagy inhibitor 3-methyladenine and mimicked by the autophagy agonist rapamycin. In control SH-SY5Y cells, HPC upregulated the expression of HIF-1α and downstream molecules such as BNIP3 and Beclin1. Additionally, HPC increased the LC3-II/LC3-I ratio and decreased p62 levels. The increase in the LC3-II/LC3-I ratio was inhibited by the HIF-1α inhibitor YC-1 or by Beclin1-short hairpin RNA (shRNA). In OGD/R-treated SH-SY5Y cells, HPC also upregulated the expression levels of HIF-1α, BNIP3, and Beclin1, as well as the LC3-II/LC3-I ratio. Furthermore, YC-1 or Beclin1-shRNA attenuated the HPC-mediated cell viability in OGD/R-treated cells. Taken together, our results demonstrate that HPC protects SH-SY5Y cells against OGD/R via HIF-1α/Beclin1-regulated autophagy.

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BNIP3 mediates pre‐myelinating oligodendrocyte cell death in hypoxia and ischemia

Cited by 28 publications

References 26 publications

Roles of NG2‐glia in ischemic stroke

Roles of NG2‐glia in ischemic stroke

Monocarboxylate transporter 1 and the vulnerability of oligodendrocyte lineage cells to metabolic stresses

HIF-1α/Beclin1-Mediated Autophagy Is Involved in Neuroprotection Induced by Hypoxic Preconditioning

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