ArticleJournal of neuroinflammation2014
The role of aquaporin 4 in apoptosis after intracerebral hemorrhage.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- Aquaporin-4 suppresses neuronal pyroptosis after ischemic stroke via the IκBα/NF-κB signaling pathway.Frontiers in immunology · 2026Article
- Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies.Biomedicines · 2025Review
- Viral immunological complications in neurological surgery: A comprehensive review of homeostatic disturbances and cognitive impairments.Surgical neurology international · 2025Review
- Ion Channel Dysregulation Following Intracerebral Hemorrhage.Neuroscience bulletin · 2024Review
- Astrocytes in intracerebral hemorrhage: impact and therapeutic objectives.Frontiers in molecular neuroscience · 2024Review
- Connexin 43 Promotes Neurogenesis via Regulating Aquaporin-4 after Cerebral Ischemia.Neurotoxicity research · 2023Article
- Glymphatic system: an emerging therapeutic approach for neurological disorders.Frontiers in molecular neuroscience · 2023Review
- Methods for studying mammalian aquaporin biology.Biology methods & protocols · 2023Review
- Cholesterol efflux regulator ABCA1 exerts protective role against high shear stress-induced injury of HBMECs via regulating PI3K/Akt/eNOS signaling.BMC neuroscience · 2022Article
- Differentially Aquaporin 5 Expression in Submandibular Glands and Cerebral Cortex in Alzheimer's Disease.Biomedicines · 2022Article
- TNF-α induces AQP4 overexpression in astrocytes through the NF-κB pathway causing cellular edema and apoptosis.Bioscience reports · 2022Article
- Aquaporin-4 and Cognitive Disorders.Aging and disease · 2022Review
- Therapeutic strategies for intracerebral hemorrhage.Frontiers in neurology · 2022Review
- The stress hyperglycemia ratio predicts early hematoma expansion and poor outcomes in patients with spontaneous intracerebral hemorrhage.Therapeutic advances in neurological disorders · 2022Article
- Modes of Brain Cell Death Following Intracerebral Hemorrhage.Frontiers in cellular neuroscience · 2022Review
- Aquaporin 4 Depolarization-Enhanced Transferrin Infiltration Leads to Neuronal Ferroptosis after Subarachnoid Hemorrhage in Mice.Oxidative medicine and cellular longevity · 2022Article
- Secondary Brain Injury by Oxidative Stress After Cerebral Hemorrhage: Recent Advances.Frontiers in cellular neuroscience · 2022Review
- The relationship of α-hydroxybutyrate dehydrogenase with 1-year outcomes in patients with intracerebral hemorrhage: A retrospective study.Frontiers in neurology · 2022Article
- Circulating AQP4 Levels in Patients with Cerebral Amyloid Angiopathy-Associated Intracerebral Hemorrhage.Journal of clinical medicine · 2021Article
- MR-Imaging and Histopathological Diagnostic Work-Up of Patients with Spontaneous Lobar Intracerebral Hemorrhage: Results of an Institutional Prospective Registry Study.Diagnostics (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe previously reported that aquaporin-4 deletion (AQP4-/-) in mice increased edema and altered blood-brain barrier integrity following intracerebral hemorrhage (ICH). To date, little is known about the role of AQP4 in apoptosis after ICH. The purpose of this study was to examine the role of AQP4 in apoptosis and its mechanisms after ICH using AQP4-/- mice.
methodsWe compared the survival rate and neurological deficits in wild-type (AQP4+/+) mice with those in AQP4-/- mice following ICH. Histological changes were detected with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining and Hoechst staining. The cell types involved were determined by immunocytochemical studies. We also measured activated caspase-3, caspase-9, caspase-8, Bax, and Bcl-2 with Western blotting at 1, 3, and 7 days after ICH. A cytokine protein assay was used to detect cytokines in AQP4+/+ and AQP4-/- mice following ICH, and the results were verified by ELISA.
resultsWe found more apoptotic cells in AQP4-/- mice following ICH; the cell types involved were predominantly neurons and astrocytes. Western blotting showed that the expression of activated caspase-3 and caspase-8 was significantly increased (P <0.05). Moreover, we demonstrated a greater enhancement in the release of TNF-α and IL-1β, as well as their receptors, in AQP4-/- mice following ICH than in AQP4+/+ mice by cytokine protein assay and Western blotting (P <0.05). The inhibitors of TNF-α and IL-1β reduced apoptotic cells after ICH in AQP4-/- mice compared with wild-type mice (P <0.05).
conclusionsAQP4 deletion increases apoptosis following ICH, and the underlying mechanism may be through cytokines, especially TNF-α and IL-1β, initiating the apoptotic cascade, as well as activation of caspase-3 and caspase-8.
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