MicroRNA‑155 contributes to the occurrence of epilepsy through the PI3K/Akt/mTOR signaling pathway
Open accessAbstract
Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression of microRNA-155 in patients with temporal lobe epilepsy. Commercial kit and western blot analysis were used to measure gap-associated protein expression. The aim of the present study was to investigate the effect of microRNA‑155 (miRNA‑155) in the occurrence of epilepsy and the molecular mechanism involved. In patients with temporal lobe epilepsy, miRNA‑155 expression was evidently higher than that in patients of the normal volunteers group. Overexpression of miRNA‑155 resulted in decreased brain‑derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) protein expression, increased caspase‑3 activity, tumor protein p53 (p53) and apoptosis regulator BAX (Bax) protein expression, and inhibited phosphoinositide 3‑kinase (PI3K), phosphorylated (p‑)protein kinase B (Akt) and p‑mechanistic target of rapamycin (mTOR) protein expression in epilepsy cells. PI3K inhibitor accelerated the effect of miRNA‑155 on the inhibition of BDNF and TrkB protein expression, the promotion of caspase‑3 activity, p53 and Bax protein expression, and the inhibition of PI3K, p‑Akt and p‑mTOR protein expression in epilepsy cells. The present findings indicate that miRNA‑155 contributes to the occurrence of epilepsy through the PI3K/Akt/mTOR signaling pathway.
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miR-155 regulates mTOR levels in TLE patient tissue and mouse models.
“A third study aimed at identifying a mechanism impacted by miR-155 expression, where miR-155 was identified to regulate on mTOR levels in TLE patient tissue and mouse models.”
From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [61]
The Results section, “Overexpression of miRNA-155 inhibits mTOR protein expression” (page unavailable), reports that miRNA-155 overexpression suppressed p-mTOR in glutamate-stimulated hT22 cells. The patient results report elevated miRNA-155 expression in temporal lobe epilepsy, not regulation of mTOR in patient tissue. The cited passages do not report an experiment in mouse models. (LLM, conf=0.90)
Experimental — accuracy not yet measuredmiR-155 expression modulates BDNF and TrkB expression.
“Expression of miR-155 modulated expression of BDNF and TrkB [61]”
From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [61]
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Aloi, M. S., Prater, K. E., Sánchez, R. E. A., Beck, A., Pathan, J. L., Davidson, S., Wilson, A., Keene, C. D., de la Iglesia, H., Jayadev, S., et al. (2023) · Journal of Neuroinflammation · doi:10.1186/s12974-023-02745-6 · Cited by 43 · see citing works
- Authors
- Duan, W., Chen, Y., & Wang, X.
- Affiliations
- Harbin Medical University (CN)
- Daqing Oilfield General Hospital (CN)
- Department of Neurology, Ya'an Hospital, Ya'an, Sichuan 625000, P.R. China
- Venue
- International Journal of Molecular Medicine
- Publisher
- Spandidos Publications
- Published
- 2018-06-01
- Volume
- 42
- Issue
- 3
- Pages
- 1577-1584
- ISSN
- 1107-3756 (ISSN-L)
- 1791-244X
- OpenAlex
- W2806206195
- Cited by
- 61
- References
- 0
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 14 · 2023: 8 · 2022: 9 · 2021: 9 · 2020: 7 · 2019: 4 · 2018: 1
- FWCI
- 4.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Pharmacological Effects and Toxicity Studies
- Keywords
- miR-155, temporal lobe epilepsy, PI3K/AKT/mTOR pathway, brain-derived neurotrophic factor, TrkB, caspase-3, p53, Bax, apoptosis, PI3K inhibitors
- MeSH terms
- Aged, Animals, Cell Line, Epilepsy, Humans, Signal Transduction, Tumor Suppressor Protein p53, Brain-Derived Neurotrophic Factor, Phosphatidylinositol 3-Kinases, Receptor, trkB, MicroRNAs, bcl-2-Associated X Protein, Proto-Oncogene Proteins c-akt, Mice, Caspase 3, TOR Serine-Threonine Kinases
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