ArticleMolecular therapy. Nucleic acids2020
MEL Ameliorates Post-SAH Cerebral Vasospasm by Affecting the Expression of eNOS and HIF1α via H19/miR-138/eNOS/NO and H19/miR-675/HIF1α.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 22 citations in OpenAlex.
- A Preliminary Study of Effect of Melatonin on Inflammation and Hypoxia-Related Factors in a Mouse Model of Elastase-Induced Intracranial Aneurysm.Brain and behavior · 2025Article
- The Role of miRNAs in Aneurysmal Subarachnoid Hemorrhage.Current molecular medicine · 2025Review
- Role of S100 and YKL40 on Intraventricular Cerebral Hemorrhages in the Preterm Infant and the Neuroprotective Role of miR-138- siRNAs-HIF-1a and miR-21-siRNAs-HVCN1 in Neonatal Mice with Nerve Injury.Current medicinal chemistry · 2024Article
- Melatonin as an Antioxidant Agent in Stroke: An Updated Review.Aging and disease · 2022Review
- Ophiopogon Polysaccharide Liposome Regulated the Immune Activity of Kupffer Cell through miR-4796.International journal of molecular sciences · 2022Article
- The multifaceted actions of the lncRNA H19 in cardiovascular biology and diseases.Clinical science (London, England : 1979) · 2022Review
- Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury.Frontiers in aging neuroscience · 2022Review
- Long non-coding RNA CCDC144NL-AS1 promotes cell proliferation by regulating the miR-363-3p/GALNT7 axis in colorectal cancer.Journal of Cancer · 2022Article
- BMSCs Regulate Astrocytes through TSG-6 to Protect the Blood-Brain Barrier after Subarachnoid Hemorrhage.Mediators of inflammation · 2021Article
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Melatonin (MEL) has been demonstrated to exert a protective effect against subarachnoid hemorrhage (SAH), and nitric oxide (NO) has been shown to play an important role in the pathogenesis of vasospasm. This study aims to explore the underlying molecular mechanisms of MEL in the control of vasospasm following SAH. MEL administration attenuates SAH-induced vasospasm and neurobehavioral deficits. Expressions of H19, eNOS, and miR-675 are low in the SAH group, while expressions of miR-138 and HIF1α are high in the SAH group. Also, MEL treatment upon SAH rats completely restores the dysregulation of H19, eNOS, miR-675, miR-138, and HIF1α to their normal levels. Moreover, MEL dose dependently increases the luciferase activity of H19 promoter and hence the expression of H19. Additionally, H19 directly targets miR-675 and miR-138 to increase miR-675 expression and inhibit miR-138 expression. As virtual target genes of miR-675 and miR-138, respectively, HIF1α and eNOS are also regulated by the treatment with MEL. In particular, MEL treatment increases the expression of miR-675 and eNOS level while decreasing the expression of miR-138 and HIF1α in a dose dependent manner. Our study found that MEL ameliorates post-SAH vasospasm by regulating the expression of eNOS and HIF1α via the H19/miR-138/eNOS/NO and H19/miR-675/HIF1α signaling pathways.
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