ArticleJournal of molecular neuroscience : MN2013
Hemoglobin-induced nitric oxide synthase overexpression and nitric oxide production contribute to blood-brain barrier disruption in the rat.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
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- Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage.Molecules (Basel, Switzerland) · 2022Review
- The Beneficial Effect of Probiotics Supplementation on Penicillin-Induced Focal Seizure in Rats.Neurochemical research · 2022Article
- Puerarin attenuates intracerebral hemorrhage-induced early brain injury possibly by PI3K/Akt signal activation-mediated suppression of NF-κB pathway.Journal of cellular and molecular medicine · 2021Article
- Early Inflammatory Cytokine Expression in Cerebrospinal Fluid of Patients with Spontaneous Intraventricular Hemorrhage.Biomolecules · 2021Article
- Mechanisms of Oxidative Stress and Therapeutic Targets following Intracerebral Hemorrhage.Oxidative medicine and cellular longevity · 2021Review
- Application of Programmable Tetrahedral Framework Nucleic Acid-Based Nanomaterials in Neurological Disorders: Progress and Prospects.Frontiers in bioengineering and biotechnology · 2021Review
- Microglia Phenotype and Intracerebral Hemorrhage: A Balance of Yin and Yang.Frontiers in cellular neuroscience · 2021Article
- miR-183-5p alleviates early injury after intracerebral hemorrhage by inhibiting heme oxygenase-1 expression.Aging · 2020Article
- Electrohypersensitivity as a Newly Identified and Characterized Neurologic Pathological Disorder: How to Diagnose, Treat, and Prevent It.International journal of molecular sciences · 2020Review
- Interaction of Microglia and Astrocytes in the Neurovascular Unit.Frontiers in immunology · 2020Review
- Neuroinflammation after Intracerebral Hemorrhage and Potential Therapeutic Targets.Journal of stroke · 2020Review
- Lesional and perilesional tissue characterization by automated image processing in a novel gyrencephalic animal model of peracute intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
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8 authors.
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Abstract
Hemoglobin (Hb) released from extravasated erythrocytes may have a critical role in the process of blood-brain barrier (BBB) disruption and subsequent edema formation after intracerebral hemorrhage (ICH). Excessive nitric oxide (NO) production synthesized by nitric oxide synthase (NOS) has been well documented to contribute to BBB disruption. However, considerably less attention has been focused on the role of NO in Hb-induced BBB disruption. This study was designed to examine the hypothesis that Hb-induced NOS overexpression and excessive NO production may contribute to the changes of tight junction (TJ) proteins and subsequent BBB dysfunction. Hemoglobin was infused with stereotactic guidance into the right caudate nucleus of male Sprague Dawley rats. Then, we investigated the effect of Hb on the BBB permeability, changes of TJ proteins (claudin-5, occludin, zonula occludens-1 (ZO-1), and junctional adhesion molecule-1 (JAM-1)), iron deposition, expression of inducible NOS (iNOS) and endothelial NOS (eNOS), as well as NO production. Hb injection caused a significant increase in BBB permeability. Significant reduction of claudin-5, ZO-1, and JAM-1 was observed after Hb injection as evidenced by PCR and immunofluorescence. After a decrease at early stage, occludin showed a fivefold increase in mRNA level at 7 days. Significant iron deposition was detectable from 48 h to 7 days in a time-dependent manner. The iNOS and eNOS levels dramatically increased after Hb injection concomitantly with large quantities of NO released. Furthermore, enhanced iNOS or eNOS immunoreactivity was co-localized with diffused or diminished claudin-5 staining. We concluded that overexpressed NOS and excessive NO production induced by Hb may contribute to BBB disruption, which may provide an important potential therapeutic target in the treatment of ICH.
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