ArticleThe Journal of clinical investigation2022
NOGOB receptor deficiency increases cerebrovascular permeability and hemorrhage via impairing histone acetylation-mediated CCM1/2 expression.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Human stem cell models in cerebral cavernous malformations.Stem cell research & therapy · 2026Review
- An EGFR co-amplified lncRNA HELDR promotes glioblastoma malignancy through KAT7-driven gene programs.Nature cell biology · 2026Article
- Targeting epigenetic remodeling of the blood-brain barrier: current knowledge for drug therapy.Epigenomics · 2026Review
- Sleep and circadian rhythms in cardiovascular resilience: mechanisms, implications, and a Roadmap for research and interventions.Nature reviews. Cardiology · 2026Review
- Histone and non-histone (de)acetylation impact on the blood-brain barrier.Fluids and barriers of the CNS · 2026Review
- Enterococcus-derived cytolysin exacerbates ischemic stroke by disrupting the blood-brain barrier via NLRP3 activation.Journal of neuroinflammation · 2025Article
- Glucose transporter 1 is essential to maintain brain endothelial cell homeostasis under hyperglycemia condition.American journal of physiology. Cell physiology · 2025Article
- Loss of NgBR causes neuronal damage through decreasing KAT7-mediated RFX1 acetylation and FGF1 expression.Cellular and molecular life sciences : CMLS · 2025Article
- Caveolae-Mediated Transcytosis and Its Role in Neurological Disorders.Biomolecules · 2025Review
- Appraising histone H4 lysine 5 lactylation as a novel biomarker in breast cancer.Scientific reports · 2025Article
- Construction of a novel platelet‑related gene risk model to predict the prognosis and drug response in virus‑related hepatocellular carcinoma.Oncology letters · 2024Article
- Insights into the regulatory role of epigenetics in moyamoya disease: Current advances and future prospectives.Molecular therapy. Nucleic acids · 2024Review
- Novel Factors Regulating Proliferation, Migration, and Differentiation of Fibroblasts, Keratinocytes, and Vascular Smooth Muscle Cells during Wound Healing.Biomedicines · 2024Review
- Trifluoperazine regulates blood-brain barrier permeability via the MLCK/p-MLC pathway to promote ischemic stroke recovery.iScience · 2024Article
- Inhibition of UTX/KDM6A improves recovery of spinal cord injury by attenuating BSCB permeability and macrophage infiltration through the MLCK/p-MLC pathway.Journal of neuroinflammation · 2023Article
- A year in review: brain barriers and brain fluids research in 2022.Fluids and barriers of the CNS · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The loss function of cerebral cavernous malformation (CCM) genes leads to most CCM lesions characterized by enlarged leaking vascular lesions in the brain. Although we previously showed that NOGOB receptor (NGBR) knockout in endothelial cells (ECs) results in cerebrovascular lesions in the mouse embryo, the molecular mechanism by which NGBR regulates CCM1/2 expression has not been elucidated. Here, we show that genetic depletion of Ngbr in ECs at both postnatal and adult stages results in CCM1/2 expression deficiency and cerebrovascular lesions such as enlarged vessels, blood-brain-barrier hyperpermeability, and cerebral hemorrhage. To reveal the molecular mechanism, we used RNA-sequencing analysis to examine changes in the transcriptome. Surprisingly, we found that the acetyltransferase HBO1 and histone acetylation were downregulated in NGBR-deficient ECs. The mechanistic studies elucidated that NGBR is required for maintaining the expression of CCM1/2 in ECs via HBO1-mediated histone acetylation. ChIP-qPCR data further demonstrated that loss of NGBR impairs the binding of HBO1 and acetylated histone H4K5 and H4K12 on the promotor of the CCM1 and CCM2 genes. Our findings on epigenetic regulation of CCM1 and CCM2 that is modulated by NGBR and HBO1-mediated histone H4 acetylation provide a perspective on the pathogenesis of sporadic CCMs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.