ArticleNeurochemical research2022
Transcription Factor HEY1 Improves Brain Vascular Endothelial Cell Function and Alleviates Ischemic Stroke by Upregulating NOTCH3.
Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- PEBP1 inhibition as a therapeutic target for neurological recovery in ischemic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Nlrc3 signaling is indispensable for hematopoietic stem cell emergence via Notch signaling in vertebrates.Nature communications · 2024Article
- Gli2-induced lncRNA Peg13 alleviates cerebral ischemia-reperfusion injury by suppressing Yy1 transcription in a PRC2 complex-dependent manner.Metabolic brain disease · 2023Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the function of hairy/enhancer-of-split related with YRPW motif protein 1 (HEY1) and Notch receptor 3 (NOTCH3) in ischemic stroke. Stroke models were established by middle cerebral artery occlusion (MCAO) and oxygen glucose deprivation (OGD) in rats and rat brain microvascular endothelial cells (BMVECs), respectively. Neurological deficit evaluation and 2,3,5-triphenyltetrazolium chloride staining were used to assess cerebral injury. The expression of HEY1 and NOTCH3 was manipulated using gain and loss of function approaches. Terminal deoxynucleotidyl transferase dUTP nick end labeling and Western blotting analysis of cleaved caspase-3 and B-cell lymphoma-2 (Bcl2) were used to evaluate apoptosis. Enzyme-linked immunosorbent assay was performed to measure the expression levels of interleukin (IL)-1β, IL-6 and IL-18. The proliferation and migration of BMVECs were analyzed by Ki-67 immunofluorescence and scratch assay, respectively. Tube formation assay was conducted to measure the length of capillary-like tubes formed by BMVECs. Co-immunoprecipitation was used to testify the relationship between HEY1 and NOTCH3. HEY1 and NOTCH3 were upregulated in MCAO and OGD models. HEY1 ameliorated ischemic injuries in MCAO rats. Knockdown of HEY1 or NOTCH3 promoted OGD-induced apoptosis and inflammation and inhibited proliferation and migration in BMVECs. NOTCH3 was a binding protein of HEY1. Overexpression of HEY1 offset the disease-promoting effect of NOTCH3 silencing. HEY1 suppresses apoptosis and inflammation and promotes proliferation and migration in BMVECs by upregulating NOTCH3, thereby ameliorating ischemic stroke.
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