ArticleBiomedical journal2023
Long non-coding RNA TTTY15 sponges miR-520a-3p to exacerbate neural apoptosis induced by cerebral ischemia/reperfusion via targeting IRF9 both in vivo and in vitro.
Article in Biomedical journal, 2023. 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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Who cites it
5 citing papers in PubMed.
- Interferon regulatory factors: the next prospective targets for tissue ischemia-reperfusion injury?Frontiers in immunology · 2026Review
- Silencing lncRNA GABPB1-AS1 alleviates cerebral ischemia reperfusion injury through the miR-641/NUCKS1 axis.American journal of translational research · 2024Article
- The Role of microRNAs in Epigenetic Regulation of Signaling Pathways in Neurological Pathologies.International journal of molecular sciences · 2023Review
- When it doesn't run in the blood(vessels) - events involved in vascular disorders.Biomedical journal · 2023Article
- Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway.Iranian journal of basic medical sciences · 2023Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStudies have proven that as competing endogenous RNAs (ceRNAs), long non-coding RNAs (lncRNAs) play vital roles in regulating RNA transcripts in ischemic stroke. It has been reported that TTTY15, a lncRNA, is dysregulated in cardiomyocytes after ischemic injury. We intended to explore the potential regulating mechanism of TTTY15 in ischemic stroke.
methodsTTTY15 and miR-520a-3p levels in vivo were measured in the cerebral ischemia/reperfusion (I/R) model. Cell apoptosis was measured by flow cytometry. To manifest TTTY15 functions in I/R injury, Neuro 2a (N2a) cells were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) and treated with si-NC, pcDNA3.1-NC, si-TTTY15 or pcDNA3.1-TTTY15.
resultsTTTY15 expression was elevated and miR-520a-3p expression was declined in mouse brains exposed to I/R and in N2a cells exposed to OGD/R. Bioinformatics analyses predicted the binding sites of miR-520a-3p in the 3'-UTRs of interferon regulatory factor 9 (IRF9) and TTTY15. Luciferase reporter assay exhibited that TTTY15 bound to miR-520a-3p directly and IRF9 was targeted by miR-520a-3p. MiR-520a-3p overexpression diminished N2a cell apoptosis caused by OGD/R. TTTY15 overexpression antagonized the inhibitory impacts of miR-520a-3p on IRF9 expression and apoptosis after OGD/R, while TTTY15 knockdown enhanced the inhibitory impacts of miR-520a-3p. Additionally, TTTY15 knockdown alleviated brain damages and neurological deficits induced by I/R in vivo. Our results revealed that TTTY15 modulated IRF9 via acting as a ceRNA for miR-520a-3p.
conclusionThe study revealed the roles of TTTY15/miR-520a-3p/IRF9 signaling pathway in regulating cerebral ischemia/reperfusion injury.
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