ArticleCell cycle (Georgetown, Tex.)2021
ZEB2, interacting with MDM2, contributes to the dysfuntion of brain microvascular endothelial cells and brain injury after intracerebral hemorrhage.
Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- MDM2-GPX4-ferroptosis regulatory axis exerts neurotoxic effects in intracerebral hemorrhage.Neural regeneration research · 2026Article
- Zinc finger proteins (ZFPs) in health and disease.Molecular biomedicine · 2026Review
- Article
- ZEB2 reduction contributes to pre-eclampsia via Wnt/β-Catenin pathway.Cell division · 2024Article
- Knockdown of LCN2 Attenuates Brain Injury After Intracerebral Hemorrhage via Suppressing Pyroptosis.Neuropsychiatric disease and treatment · 2024Article
- BCL-3 Promotes Intracerebral Hemorrhage Progression by Increasing Blood-Brain Barrier Permeability, Inflammation, and Cell Apoptosis via Endoplasmic Reticulum Stress.Mediators of inflammation · 2023Article
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Authors and funding
6 authors.
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Abstract
ZEB2 has been shown to be upregulated in the brain tissues of rats with intracerebral hemorrhage (ICH), but its role in ICH-caused brain injury remains unclear. Here, an ICH rat model was established via intracerebral injection of autologous blood, and the lentivirus-mediated ZEB2 short hairpin RNA (sh-ZEB2) or negative control (scramble) were administered 0.5 hours after ICH. Silencing ZEB2 alleviated ICH-induced neurologic deficits and the increase of BBB permeability, brain water content and ZEB2 expression. Next, OGD (oxygen glucose deprivation) plus hemin was used to treat primary brain microvascular endothelial cells (BMECs) to simulate the ICH condition
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