LncRNA-SNHG3 promotes neuroinflammation post-intracerebral hemorrhage by regulating the miR-106b-5p/TXNIP axis

Background Intracerebral hemorrhage (ICH) stands as the most fatal stroke subtype, lacking any specific therapeutic approach yielding benefits for functional recovery. Objectives We aimed to explore the involvement of long non-coding RNA small nucleolar RNA host gene 3 (lncRNA-SNHG3) in post-ICH neu...

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Bibliographic Details
Published in:Molecular & cellular toxicology 2024, 20(4), , pp.883-894
Main Authors: Zhou, Fenggang, Wu, Fei, Wang, Xinran, Yu, Shihua, Tian, Wenqi, Lv, Ou
Format: Article
Language:English
Subjects:
Biomedical and Life Sciences
Brain tumors
Cell Biology
Edema
Hemorrhage
Inflammation
Life Sciences
Metastases
Non-coding RNA
Nucleoli
Original Article
Pharmacology/Toxicology
Recovery of function
snoRNA
Thioredoxin
Up-regulation
생물학
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Summary:Background Intracerebral hemorrhage (ICH) stands as the most fatal stroke subtype, lacking any specific therapeutic approach yielding benefits for functional recovery. Objectives We aimed to explore the involvement of long non-coding RNA small nucleolar RNA host gene 3 (lncRNA-SNHG3) in post-ICH neuroinflammation, offering a novel rationale for ICH treatment. Results Brain tissues of ICH-induced mice exhibited upregulated levels of lncRNA-SNHG3. Inhibition of lncRNA-SNHG3 led to reduced modified neurological severity scores, diminished brain edema, and attenuated inflammatory infiltration, coupled with reduced levels of tumor necrosis factor-α/interleukin-1β. By repressing miR-106b-5p via targeted binding, lncRNA-SNHG3 facilitated the inhibition of transcriptional and protein levels of thioredoxin-interacting protein (TXNIP) through targeted binding to TXNIP mRNA. The counteraction of miR-106b-5p inhibition or the upregulation of TXNIP reversed the ameliorative effect of sh-SNHG3 on neuroinflammation. Conclusion Competitive binding of lncRNA-SNHG3 to miR-106b-5p resulted in the upregulation of TXNIP, consequently inducing neuroinflammation and exacerbating ICH-induced damage.
ISSN:1738-642X
2092-8467
DOI:10.1007/s13273-023-00397-4