ArticleFrontiers in cellular neuroscience2019
Regulation of ADAM10 by MicroRNA-23a Contributes to Epileptogenesis in Pilocarpine-Induced Status Epilepticus Mice.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Modulation of Microglia M2 Polarization and Alleviation of Hippocampal Neuron Injury By MiR-106b-5p/RGMa in a Mouse Model of Status Epilepticus.Inflammation · 2022Article
- Aberrant expression of miRNAs in epilepsy.Molecular biology reports · 2022Review
- The Coordination of mTOR Signaling and Non-Coding RNA in Regulating Epileptic Neuroinflammation.Frontiers in immunology · 2022Review
- Review
- ADAM10 promotes cell growth, migration, and invasion in osteosarcoma via regulating E-cadherin/β-catenin signaling pathway and is regulated by miR-122-5p.Cancer cell international · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ADAM10, a member of the disintegrin and metalloproteinase domain-containing protein (ADAM) family, has been reported to mediate proteolytic shedding of cell surface proteins. An increasing body of evidence indicates that ADAM10 is involved in various neurological disorders including epilepsy. However, the molecular mechanisms underlying the regulation of ADAM10 expression in the epileptic brain remain poorly understood. In this study, we demonstrate that ADAM10 is targeted by microRNA-23a (miR-23a) in the hippocampus. Inhibition of miR-23a increased hippocampal ADAM10 expression while an increase in miR-23a suppressed hippocampal ADAM10 expression in pilocarpine-induced status epilepticus (SE) mice. Furthermore, inhibition of miR-23a suppressed spontaneous recurrent seizures through up-regulation of ADAM10 in pilocarpine-induced SE mice. Our findings suggest that miR-23a targeting of ADAM10 contributes to epileptogenesis in temporal lobe epilepsy. Thus, the miR-23a-ADAM10 pathway in the epileptic brain may provide a novel target for the treatment of epilepsy.
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Registered trials
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