ArticleTranslational stroke research2014
Tenascin-C causes neuronal apoptosis after subarachnoid hemorrhage in rats.
Article in Translational stroke research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 65 citations in OpenAlex.
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Involvement of Periostin in Acute Neuronal Apoptosis Induced by Subarachnoid Hemorrhage in Mice and its Suppression by Clarithromycin.Neurocritical care · 2025Article
- A neuroprotective tetrapeptide for treatment of acute traumatic brain injury.EMBO molecular medicine · 2025Article
- Tremella fuciformis Polysaccharides Alleviate Early Brain Injury in Experimental Subarachnoid Hemorrhage by Inhibiting the KDR-Mediated P38 MAPK/NF-κB Pathway.Molecular neurobiology · 2025Article
- The Effect of Fibulin-5 on Hydrocephalus After Subarachnoid Hemorrhage in Mice.International journal of molecular sciences · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Tenascin-C Facilitates Microglial Polarization via TLR4/MyD88/NF-κB Pathway Following Subarachnoid Hemorrhage.Journal of inflammation research · 2025Article
- Tenascin-C as a Target for Intervention in Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.Acta neurochirurgica. Supplement · 2025Review
- Tenascin C activates the toll‑like receptor 4/NF‑κB signaling pathway to promote the development of polycystic ovary syndrome.Molecular medicine reports · 2024Article
- Anti-Apoptotic Effects of AMPA Receptor Antagonist Perampanel in Early Brain Injury After Subarachnoid Hemorrhage in Mice.Translational stroke research · 2024Article
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Tenascin-C induction exacerbates post-stroke brain damage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Matricellular protein tenascin C: Implications in glioma progression, gliomagenesis, and treatment.Frontiers in oncology · 2022Review
- Progress in mimicking brain microenvironments to understand and treat neurological disorders.APL bioengineering · 2021Article
- The Pathogenesis of Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2021Review
- Generation of Transgenic Mice that Conditionally Overexpress Tenascin-C.Frontiers in immunology · 2021Article
- Knock-Out of Tenascin-C Ameliorates Ischemia-Induced Rod-Photoreceptor Degeneration and Retinal Dysfunction.Frontiers in neuroscience · 2021Article
- Mechanisms of neuroinflammation and inflammatory mediators involved in brain injury following subarachnoid hemorrhage.Histology and histopathology · 2020Review
- The Role of Tenascin-C in Tissue Injury and Repair After Stroke.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of tenascin-C (TNC), a matricellular protein, in brain injury is unknown. The aim of this study was to examine if TNC causes neuronal apoptosis after subarachnoid hemorrhage (SAH), a deadly cerebrovascular disorder, using imatinib mesylate (a selective inhibitor of platelet-derived growth factor receptor [PDGFR] that is reported to suppress TNC induction) and recombinant TNC. SAH by endovascular perforation caused caspase-dependent neuronal apoptosis in the cerebral cortex irrespective of cerebral vasospasm development at 24 and 72 h post-SAH, associated with PDGFR activation, mitogen-activated protein kinases (MAPKs) activation, and TNC induction in rats. PDGFR inactivation by an intraperitoneal injection of imatinib mesylate prevented neuronal apoptosis, as well as MAPKs activation and TNC induction in the cerebral cortex at 24 h. A cisternal injection of recombinant TNC reactivated MAPKs and abolished anti-apoptotic effects of imatinib mesylate. The TNC injection also induced TNC itself in SAH brain, which may internally augment neuronal apoptosis after SAH. These findings suggest that TNC upregulation by PDGFR activation causes neuronal apoptosis via MAPK activation, and that the positive feedback mechanisms may exist to augment neuronal apoptosis after SAH. TNC-induced neuronal apoptosis would be a new target to improve outcome after SAH.
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