ArticleScientific reports2021
Gene expression profiling of brain endothelial cells after experimental subarachnoid haemorrhage.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Epigenome-wide DNA methylation profiling in aneurysmal subarachnoid hemorrhage and delayed ischemic neurologic deficit: a prospective observational study.International journal of surgery (London, England) · 2026Observational
- Gene expression changes in human cerebral arteries following hemoglobin exposure: implications for vascular responses in SAH.Frontiers in physiology · 2025Article
- A nomogram model for predicting postoperative prognosis in patients with aneurysmal subarachnoid hemorrhage using preoperative biochemical indices.BMC neurology · 2024Article
- Cerebrolysin in Patients with Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis.Journal of clinical medicine · 2023Review
- Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2023Review
- Subarachnoid hemorrhage triggers neuroinflammation of the entire cerebral cortex, leading to neuronal cell death.Inflammation and regeneration · 2022Article
- Oxidative Stress and the Neurovascular Unit.Life (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Subarachnoid haemorrhage (SAH) is a type of hemorrhagic stroke that is associated with high morbidity and mortality. New effective treatments are needed to improve outcomes. The pathophysiology of SAH is complex and includes early brain injury and delayed cerebral ischemia, both of which are characterized by blood-brain barrier (BBB) impairment. We isolated brain endothelial cells (BECs) from mice subjected to SAH by injection of blood into the prechiasmatic cistern. We used gene expression profiling to identify 707 unique genes (2.8% of transcripts, 403 upregulated, 304 downregulated, 24,865 interrogated probe sets) that were significantly differentially expressed in mouse BECs after SAH. The pathway involving prostaglandin synthesis and regulation was significantly upregulated after SAH, including increased expression of the Ptgs2 gene and its corresponding COX-2 protein. Celecoxib, a selective COX-2 inhibitor, limited upregulation of Ptgs2 in BECs. In this study, we have defined the gene expression profiling of BECs after experimental SAH and provide further insight into BBB pathophysiology, which may be relevant to other neurological diseases such as traumatic brain injury, brain tumours, ischaemic stroke, multiple sclerosis, and neurodegenerative disorders.
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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.