ArticleMolecular neurodegeneration2015
MicroRNA-9 induces defective trafficking of Nav1.1 and Nav1.2 by targeting Navβ2 protein coding region in rat with chronic brain hypoperfusion.
Article in Molecular neurodegeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
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- LncRNA MALAT1 Targets miR-9-3p to Upregulate SAP97 in the Hippocampus of Mice with Vascular Dementia.Biochemical genetics · 2023Article
- MiR-322-5p Alleviates Cell Injury and Impairment of Cognitive Function in Vascular Dementia by Targeting TSPAN5.Yonsei medical journal · 2022Article
- MiR-9-5p Regulates Genes Linked to Cerebral Calcification in the Osteogenic Differentiation Model and Induces Generalized Alteration in the Ion Channels.Journal of molecular neuroscience : MN · 2021Article
- Biologic Therapy in Chronic Pain Management: a Review of the Clinical Data and Future Investigations.Current pain and headache reports · 2021Review
- Regulatory microRNAs and vascular cognitive impairment and dementia.CNS neuroscience & therapeutics · 2020Review
- Therapeutic and Diagnostic Potential of microRNAs in Vascular Cognitive Impairment.Journal of molecular neuroscience : MN · 2020Review
- MicroRNA-153 impairs presynaptic plasticity by blocking vesicle release following chronic brain hypoperfusion.Cell communication and signaling : CCS · 2020Article
- MiR-206 inhibits epilepsy and seizure-induced brain injury by targeting CCL2.Cytotechnology · 2019Article
- Regulation of Ion Channels by MicroRNAs and the Implication for Epilepsy.Current neurology and neuroscience reports · 2018Review
- ABCC10 Plays a Significant Role in the Transport of Gefitinib and Contributes to Acquired Resistance to Gefitinib in NSCLC.Frontiers in pharmacology · 2018Article
- MicroRNA-195 prevents dendritic degeneration and neuron death in rats following chronic brain hypoperfusion.Cell death & disease · 2017Article
- The influence of sodium on pathophysiology of multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies have demonstrated that the trafficking defects of Nav1.1/Nav1.2 are involved in the dementia pathophysiology. However, the detailed mechanisms are not fully understood. Moreover, whether the impaired miRNAs regulation linked to dementia is a key player in sodium channel trafficking disturbance remains unclear. The cognitive impairment induced by chronic cerebral ischemia through chronic brain hypoperfusion (CBH) is likely reason to precede dementia. Therefore, our goal in the present study was to examine the role of microRNA-9 (miR-9) in regulating Nav1.1/Nav1.2 trafficking under CBH generated by bilateral common carotid artery occlusion (2VO).
resultsThe impairment of Nav1.1/Nav1.2 trafficking and decreased expression of Navβ2 were found in the hippocampi and cortices of rats following CBH generated by bilateral 2VO. MiR-9 was increased in both the hippocampi and cortices of rats following CBH by qRT-PCR. Intriguingly, miR-9 suppressed, while AMO-miR-9 enhanced, the trafficking of Nav1.1/Nav1.2 from cytoplasm to cell membrane. Further study showed that overexpression of miR-9 inhibited the Navβ2 expression by targeting on its coding sequence (CDS) domain by dual luciferase assay. However, binding-site mutation or miR-masks failed to influence Navβ2 expression as well as Nav1.1/Nav1.2 trafficking process, indicating that Navβ2 is a potential target for miR-9. Lentivirus-mediated miR-9 overexpression also inhibited Navβ2 expression and elicited translocation deficits to cell membrane of Nav1.1/Nav1.2 in rats, whereas injection of lentivirus-mediated miR-9 knockdown could reverse the impaired trafficking of Nav1.1/Nav1.2 triggered by 2VO.
conclusionsWe conclude that miR-9 may play a key role in regulating the process of Nav1.1/Nav1.2 trafficking via targeting on Navβ2 protein in 2VO rats at post-transcriptional level, and inhibition of miR-9 may be a potentially valuable approach to prevent Nav1.1/Nav1.2 trafficking disturbance induced by CBH.
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