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Updated: Apr 5, 2026
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
Published on: June 20, 2025
[Prediction of regulating network of innate immune signaling molecule hsa-miR-181a in stroke development based on
Yanni Lyu1, Yisong Qian2, Longsheng Fu1
1Department of Pharmacy, First Affiliated Hospital, Nanchang University, Nanchang 330046, China, China.
Objective:
To predict the regulating network of innate immunity signaling molecule hsa-miR-181a in stroke based on the methods of bioinformatics.
Methods:
The UCSC genome browser, the human miRNA disease database (HMDD), the transcription factor-miRNA regulation database (TransmiR), the database on predicted and validated miRNA targets (miRwalk), the Genecards, the long non-coding RNA (LncRNA) disease database, the DIANA LAB-LncBase and the ConSite were employed to study the upstream transcription factor, downstream target genes and the interactive LncRNA of hsa-miR-181a and to draw the core regulating network of hsa-miR-181a. To verify the hsa-miR-181a regulating network, we used lipopolysaccharide (LPS) to stimulate the BV2 cells transfected by lentivirus and real-time quantitative PCR to detect the changes of Toll-like receptor 4 (TLR4), tumor protein 63 (p63), miR-181a and nuclear factor κB (NF-κB) p65.
Results:
The UCSC genome browser showed that hsa-miR-181a had two subtypes, which were demonstrated with high conservatism in several species. Diseases analysis and literatures investigation revealed that the hsa-miR-181a was related with many diseases, especially ischemia diseases. Bioinformatics analysis indicated that hsa-miR-181a was regulated by the transcription factors p63, and at the same time, it could regulate 58 target genes such as brain-derived neurotrophic factor (BDNF), TLR4 etc. IncRNA CDKN2B-AS1 and its transcription factors Snail and n-MYC might also interact with hsa-miR-181a. All the relative genes composed a regulatory network with hsa-miR-181a as a core and played important roles in the process of stroke. In LPS-stimulated BV2 cells, the expression levels of TLR4, p63, miR-181a were up-regulated; while the levels of p63, miR-181a and NF-κB p65 decreased in the lentivirus-infected BV2 cells, indicating that p63 was the key signaling molecule in the process of TLR4 regulating miR-181a.
Conclusion:
The bioinformatics analysis and preliminary experimental verification predicted and demonstrated the regulating network of hsa-miR-181a in stroke.
