ArticleFrontiers in molecular neuroscience2016
Cerebral Microvascular Endothelial Cell Apoptosis after Ischemia: Role of Enolase-Phosphatase 1 Activation and Aci-Reductone Dioxygenase 1 Translocation.
Article in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
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- Indispensable role of AcrEF in modulating Salmonella virulence and disrupting host tight junctions to facilitate paracellular entry and invasion.Biology direct · 2025Article
- Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Article
- Comprehensive pan-cancer analysis of ENOPH1 in human tumors.Discover oncology · 2025Article
- Non-Targeted Metabolomics Analysis of Small Molecular Metabolites in Refrigerated Goose Breast Meat.Veterinary sciences · 2024Article
- The Role of Gut Microbiota in Blood-Brain Barrier Disruption after Stroke.Molecular neurobiology · 2024Review
- Mutations in ARHGEF15 cause autosomal dominant hereditary cerebral small vessel disease and osteoporotic fracture.Acta neuropathologica · 2023Article
- Advancement in CRISPR/Cas9 Technology to Better Understand and Treat Neurological Disorders.Cellular and molecular neurobiology · 2023Review
- Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022Review
- Proton exchange rate of chemical exchange saturation transfer MRI constructed from direct saturation-removed omega plots to improve the assessment of patients with ischemic stroke.Quantitative imaging in medicine and surgery · 2022Article
- Caspase-1: A Promising Target for Preserving Blood-Brain Barrier Integrity in Acute Stroke.Frontiers in molecular neuroscience · 2022Review
- A novel brain targeted plasma exosomes enhance the neuroprotective efficacy of edaravone in ischemic stroke.IET nanobiotechnology · 2021Article
- Cerebral Edema Formation After Stroke: Emphasis on Blood-Brain Barrier and the Lymphatic Drainage System of the Brain.Frontiers in cellular neuroscience · 2021Review
- LncRNA MALAT1 Promotes OGD-Induced Apoptosis of Brain Microvascular Endothelial Cells by Sponging miR-126 to Repress PI3K/Akt Signaling Pathway.Neurochemical research · 2020Article
- Buyang Huanwu Decoction Promotes Angiogenesis after Cerebral Ischemia by Inhibiting the Nox4/ROS Pathway.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Dl-3-n-butylphthalide Reduces Neurovascular Inflammation and Ischemic Brain Injury in Mice.Aging and disease · 2019Article
- Human acireductone dioxygenase (HsARD), cancer and human health: Black hat, white hat or gray?Inorganics · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enolase-phosphatase 1 (ENOPH1), a newly discovered enzyme of the methionine salvage pathway, is emerging as an important molecule regulating stress responses. In this study, we investigated the role of ENOPH1 in blood brain barrier (BBB) injury under ischemic conditions. Focal cerebral ischemia induced ENOPH1 mRNA and protein expression in ischemic hemispheric microvessels in rats. Exposure of cultured brain microvascular endothelial cells (bEND3 cells) to oxygen-glucose deprivation (OGD) also induced ENOPH1 upregulation, which was accompanied by increased cell death and apoptosis reflected by increased 3-(4, 5-Dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide formation, lactate dehydrogenase release and TUNEL staining. Knockdown of ENOPH1 expression with siRNA or overexpressing ENOPH1 with CRISPR-activated plasmids attenuated or potentiated OGD-induced endothelial cell death, respectively. Moreover, ENOPH1 knockdown or overexpression resulted in a significant reduction or augmentation of reactive oxygen species (ROS) generation, apoptosis-associated proteins (caspase-3, PARP, Bcl-2 and Bax) and Endoplasmic reticulum (ER) stress proteins (Ire-1, Calnexin, GRP78 and PERK) in OGD-treated endothelial cells. OGD upregulated the expression of ENOPH1's downstream protein aci-reductone dioxygenase 1 (ADI1) and enhanced its interaction with ENOPH1. Interestingly, knockdown of ENOPH1 had no effect on OGD-induced ADI1 upregulation, while it potentiated OGD-induced ADI1 translocation from the nucleus to the cytoplasm. Lastly, knockdown of ENOPH1 significantly reduced OGD-induced endothelial monolayer permeability increase. In conclusion, our data demonstrate that ENOPH1 activation may contribute to OGD-induced endothelial cell death and BBB disruption through promoting ROS generation and the activation of apoptosis associated proteins, thus representing a new therapeutic target for ischemic stroke.
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