ArticleMolecular neurobiology2017
Downregulation of Aquaporin-4 Protects Brain Against Hypoxia Ischemia via Anti-inflammatory Mechanism.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Acupuncture improves blood-brain barrier integrity through multi-targeted mechanisms: a preclinical meta-analysis.Frontiers in neurology · 2025Pooled it
- Histone and non-histone (de)acetylation impact on the blood-brain barrier.Fluids and barriers of the CNS · 2026Review
- Thymosin β4 stabilizes hypoxia induced brain microvascular endothelial cell dysfunction through S1PR1 dependent mechanisms.Scientific reports · 2025Article
- Umbilical Cord Blood Endothelial Progenitor Cells Modulate Neurovascular Unit Damage in a Neonatal Rat Model of Hypoxia Ischemia.Stem cell reviews and reports · 2025Article
- Targeting Aquaporin-5 by Phosphodiesterase 4 Inhibition Offers New Therapeutic Opportunities for Ovarian Ischemia Reperfusion Injury in Rats.Reproductive sciences (Thousand Oaks, Calif.) · 2024Article
- Non-coding RNAs and Aquaporin 4: Their Role in the Pathogenesis of Neurological Disorders.Neurochemical research · 2024Review
- The deletion of AQP4 and TRPV4 affects astrocyte swelling/volume recovery in response to ischemia-mimicking pathologies.Frontiers in cellular neuroscience · 2024Article
- Aquaporins: Potential Targets in Inflammatory Diseases.The Eurasian journal of medicine · 2023Article
- Leukemia-derived Exosomes Can Induce Responses Related to Tumorigenesis on Non-tumoral Astrocytes.Applied biochemistry and biotechnology · 2023Article
- Astaxanthin ameliorates spinal cord edema and astrocyte activation via suppression of HMGB1/TLR4/NF-κB signaling pathway in a rat model of spinal cord injury.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Evaluation of dual potentiality of 2,4,5-trisubstituted oxazole derivatives as aquaporin-4 inhibitors and anti-inflammatory agents in lung cells.RSC advances · 2023Article
- Edema after CNS Trauma: A Focus on Spinal Cord Injury.International journal of molecular sciences · 2023Review
- DTI-ALPS: An MR biomarker for motor dysfunction in patients with subacute ischemic stroke.Frontiers in neuroscience · 2023Article
- Alteration of the translational readthrough isoform AQP4ex induces redistribution and downregulation of AQP4 in human glioblastoma.Cellular and molecular life sciences : CMLS · 2022Article
- Aquaporin-4 Gene Polymorphisms in Relapsing Inflammatory Optic Neuropathy and RANKL in Glioblastoma: Research and Progress on Biomarkers.Noro psikiyatri arsivi · 2021Article
- Hypertonic saline improves brain edema resulting from traumatic brain injury by suppressing the NF-κB/IL-1β signaling pathway and AQP4.Experimental and therapeutic medicine · 2020Article
- Role of Aquaporins in Inflammation-a Scientific Curation.Inflammation · 2020Review
- The innate immune system and neurogenesis as modulating mechanisms of electroconvulsive therapy in pre-clinical studies.Journal of psychopharmacology (Oxford, England) · 2020Review
- Isoflurane exposure in infant rats acutely increases aquaporin 4 and does not cause neurocognitive impairment.Bosnian journal of basic medical sciences · 2019Article
- Blockade of Aquaporin 4 Inhibits Irradiation-Induced Pulmonary Inflammation and Modulates Macrophage Polarization in Mice.Inflammation · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Aquaporin-4 (AQP4), a water-channel protein, controls water fluxes into and out of the brain parenchyma. The role of AQP4 in brain edema formation and resolution remains controversial. This study therefore determined the roles of AQP4 in brain edema and explored the underlying molecular mechanism. We established hypoxia-ischemia (HI) neonatal rat model in vivo and HI cell model in vitro, which were administrated with lentiviral or shRNA vector, respectively. We found that the neurologic deficit and motor dysfunction could be induced by HI with more serious brain damage after longer HI time, and swollen cells with enlarged surrounding space were observed after HI induction. The quantity of water in the brain tissues was significantly increased in the HI rats when compared with the control group. However, the downregulation AQP4 by lentiviral or shRNA vector reversed the brain edema and neurologic deficit induced by HI. The underlying mechanism of beneficial effects of AQP4 downregulation may be due to interactive regulation of AQP4 and inflammatory cytokines including IL-1β, IL-6, IL-10, and TNFα. Our data demonstrate that the silence of AQP4 results in a significant decrease in the expression of IL-1β, IL-10, and TNFα, but had no direct effect on IL-6 expression. AQP4 could indirectly regulate the expression of IL-6 via IL-1β, IL-10, and TNFα. In summary, these findings provide a novel mechanism to explain the role of AQP4 in HI pathogenesis and are instrumental for the development of treatment for HI-induced brain edema.
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