ArticleMetabolic brain disease2023
Gli2-induced lncRNA Peg13 alleviates cerebral ischemia-reperfusion injury by suppressing Yy1 transcription in a PRC2 complex-dependent manner.
Article in Metabolic brain disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Lactylation and Ischemic Stroke: Research Progress and Potential Relationship.Molecular neurobiology · 2025Review
- The novel role of Yin Yang 1 in acute rejection of liver allografts through activation of dendritic cells.Frontiers in immunology · 2025Article
- The role of long noncoding ribonucleic acids in the central nervous system injury.Molecular and cellular biochemistry · 2024Review
- Revealing the role of Peg13: A promising therapeutic target for mitigating inflammation in sepsis.Genetics and molecular biology · 2024Article
- Regulatory RNAs: role as scaffolds assembling protein complexes and their epigenetic deregulation.Exploration of targeted anti-tumor therapy · 2024Review
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- Allelic chromatin structure precedes imprinted expression ofGenes & development · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Endothelial cell dysfunction plays an important role in cerebral ischemia-reperfusion (I/R) injury. LncRNA Peg13 is reported to be down-regulated in brain microvascular endothelial cells (BMVECs) induced by glucose-oxygen deprivation (OGD), but the mechanism of its involvement in I/R progression remains to be further explored. Here, mouse BMVECs (bEnd.3 cells) were treated with OGD / reoxygenation (OGD/R) to simulate I/R injury in vitro. Peg13 and Gli2 expression was decreased in OGD/R-treated bEnd.3 cells. And overexpression of Peg13 or Gli2 prevented OGD/R-induced reduction in cell migration and angiogenesis, as well as upregulation in cell apoptosis and oxidative stress levels. Mechanism exploration showed that Gli2 promoted the transcription of Peg13. And Peg13 repressed Yy1 transcription by binding to Ezh2 (a key subunit of PRC2 complex) and inducing the enrichment of H3K27me3 in Yy1 promoter region, thereby suppressing the transcriptional inhibition effect of Yy1 on Notch3 and promoting the expression of Notch3. Consistently, Notch3 overexpression hindered OGD/R-induced endothelium dysfunction. In addition, a brain I/R injury model was established using middle cerebral artery occlusion surgery. And lentivirus-mediated Gli2 and Peg13 overexpression vectors were injected into mice via the lateral ventricle one week before surgery. The results showed that overexpression of Peg13 or Gli2 alleviated I/R-induced neurological deficit, cerebral infarct and cerebral edema. And simultaneous overexpression of Peg13 and Gli2 showed a better protective effect than overexpression of Gli2 or Peg13 alone. In conclusion, Peg13 regulated by Gli2 inhibits Yy1 transcription in a PCR2 complex-dependent manner, and blocks the transcriptional repression of Notch3 by Yy1, thereby exerting neuroprotective effects on cerebral I/R injury.
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