ArticleScientific reports2015
Semaphorin3A elevates vascular permeability and contributes to cerebral ischemia-induced brain damage.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 75 citations in OpenAlex.
- Neuron-Derived Sema3B Facilitates Microglial Hematoma Clearance After Intracerebral Hemorrhage.Antioxidants (Basel, Switzerland) · 2026Article
- miR‑205: A dual regulator of angiogenesis in health and disease (Review).International journal of molecular medicine · 2026Review
- Inflammatory Semaphorins in the Pathogenesis and Prognosis of Acute Ischemic Stroke.Medicina (Kaunas, Lithuania) · 2025Article
- Identification and Mapping of Human Lymph Node Stromal Cell Subsets by Combining Single-Cell RNA Sequencing with Spatial Transcriptomics.European journal of immunology · 2025Article
- Molecule interacting with CasL-2 enhances tumor progression and alters radiosensitivity in cervical cancer.Journal of translational medicine · 2025Article
- Plasma Semaphorin 3A as a Potential Biomarker for Cognitive Impairment in Cerebral Small Vessel Disease.International journal of general medicine · 2025Article
- Semaphorin-3A regulates liver sinusoidal endothelial cell porosity and promotes hepatic steatosis.Nature cardiovascular research · 2024Article
- A multitrait genetic study of hemostatic factors and hemorrhagic transformation after stroke treatment.Journal of thrombosis and haemostasis : JTH · 2024Article
- Inhibition of EphA4 reduces vasogenic edema after experimental stroke in mice by protecting the blood-brain barrier integrity.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- The Involvement of Semaphorins in the Pathogenesis of Skin Diseases.International journal of molecular sciences · 2023Review
- The pulmonary vasculature in lethal COVID-19 and idiopathic pulmonary fibrosis at single-cell resolution.Cardiovascular research · 2023Article
- β-Actin: An Emerging Biomarker in Ischemic Stroke.Cellular and molecular neurobiology · 2023Review
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- Hypothermia evoked by stimulation of medial preoptic nucleus protects the brain in a mouse model of ischaemia.Nature communications · 2022Article
- An increase in Semaphorin 3A biases the axonal direction and induces an aberrant dendritic arborization in an in vitro model of human neural progenitor differentiation.Cell & bioscience · 2022Article
- Neurovascular dysfunction in GRN-associated frontotemporal dementia identified by single-nucleus RNA sequencing of human cerebral cortex.Nature neuroscience · 2022Article
- Semaphorin 3A: A potential target for prevention and treatment of nickel allergy.Communications biology · 2022Article
- Vascular Sema3E-Plexin-D1 Signaling Reactivation Promotes Post-stroke Recovery through VEGF Downregulation in Mice.Translational stroke research · 2022Article
- It takes two to tango: Widening our understanding of the onset of schizophrenia from a neuro-angiogenic perspective.Frontiers in cell and developmental biology · 2022Review
- Role of Semaphorins in Ischemic Stroke.Frontiers in molecular neuroscience · 2022Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Semaphorin 3A (Sema3A) increased significantly in mouse brain following cerebral ischemia. However, the role of Sema3A in stroke brain remains unknown. Our aim was to determine wether Sema3A functions as a vascular permeability factor and contributes to ischemic brain damage. Recombinant Sema3A injected intradermally to mouse skin, or stereotactically into the cerebral cortex, caused dose- and time-dependent increases in vascular permeability, with a degree comparable to that caused by injection of a known vascular permeability factor vascular endothelial growth factor receptors (VEGF). Application of Sema3A to cultured endothelial cells caused disorganization of F-actin stress fibre bundles and increased endothelial monolayer permeability, confirming Sema3A as a permeability factor. Sema3A-mediated F-actin changes in endothelial cells were through binding to the neuropilin2/VEGFR1 receptor complex, which in turn directly activates Mical2, a F-actin modulator. Down-regulation of Mical2, using specific siRNA, alleviated Sema3A-induced F-actin disorganization, cellular morphology changes and endothelial permeability. Importantly, ablation of Sema3A expression, cerebrovascular permeability and brain damage were significantly reduced in response to transient middle cerebral artery occlusion (tMCAO) and in a mouse model of cerebral ischemia/haemorrhagic transformation. Together, these studies demonstrated that Sema3A is a key mediator of cerebrovascular permeability and contributes to brain damage caused by cerebral ischemia.
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