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MiR-181c-5p ameliorates learning and memory in sleep-deprived mice via HMGB1/TLR4/NF-κB pathway
Abstract
Sleep deprivation (SD) can lead to cognitive impairment caused by neuroinflammation. MiR-181c-5p/HMGB1 axis plays a part in anti-inflammation effects. However, the mechanism that miR-181c-5p facilitates learning and memory in SD mice remains unclear. So we investigated the role of miR-181c-5p in learning and memory impairment induced by SD. We overexpressed miR-181c-5p in the mice hippocampus by injecting lentivirus vector-miR-181c-5p (LV-miR-181c-5p) particles. Mice were divided into four groups: control (Ctrl), SD, SD + miR-181c-5p and SD + vector. We found that mice in the third group showed ameliorated learning and memory compared with the fourth group. The content of ionized calcium binding adaptor molecule 1 (IBA-1) in the third group was decreased compared with the fourth group. Moreover, the expression levels of HMGB1, TLR4 and p-NF-κB in the hippocampus of overexpressed miR-181c-5p mice were reduced. In total, miR-181c-5p ameliorated learning and memory in SD mice via the HMGB1/TLR4/NF-κB pathway.
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“These miRNAs—miR-124-3p, miR-204-5p, miR-328-3p, and miR-181c-5p—regulate processes such as synaptic function [48–50], inflammation, and neuronal survival [51–56], which are similarly impacted by miR-129-5p [57–60] and miR-212-5p [61–66].”
From A role for astrocytic miR-129-5p in frontotemporal dementia (2025) · cites this paper as [48]
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A role for astrocytic miR-129-5p in frontotemporal dementia
Kaurani, L., Pradhan, R., Schröder, S., Burkhardt, S., Schuetz, A.-L., Krüger, D. M., Pena, T., Heutink, P., Sananbenesi, F., & Fischer, A. (2025) · Translational Psychiatry · doi:10.1038/s41398-025-03338-y · Cited by 10
Metadata
- Authors
- HU, Y., HU, C., YIN, J., ZHONG, J., DENG, Y., & YANG, G.
- Affiliations
- Central South University Xiangya School of Medicine Affiliated Haikou Hospital, China
- Venue
- Anais da Academia Brasileira de Ciências
- Publisher
- FapUNIFESP (SciELO)
- Published
- 2023
- Volume
- 95
- Issue
- suppl 1
- ISSN
- 1678-2690
- 0001-3765
- Cited by
- 4
- References
- 3
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