ArticleBrain pathology (Zurich, Switzerland)2023
Attenuation of Piwil2 induced by hypoxic postconditioning prevents cerebral ischemic injury by inhibiting CREB2 promoter methylation.
Article in Brain pathology (Zurich, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- PIWIL2 drives stroke progression via modulation of NF-κB signaling.Molecular therapy. Nucleic acids · 2026Article
- PIWI-Interacting RNAs in brain health and disease: biogenesis, mechanisms, and therapeutic horizons.Psychopharmacology · 2026Review
- Advances in basic research on post-cardiac arrest syndrome in adults: a comprehensive review.Frontiers in medicine · 2026Review
- Altered Short Non-Coding RNA Landscape in the Hippocampus of a Mouse Model of CDKL5 Deficiency Disorder.Biomolecules · 2025Article
- TET3-Interacting LncRNA TILR Is Essential for DNA Hydroxymethylation-Mediated Neuroprotection After Ischemic Stroke.Stroke · 2025Article
- Hypoxic Postconditioning Offers Neuroprotection Against Transient Cerebral Ischemia via Down-Regulation of rno_piR_011022.CNS neuroscience & therapeutics · 2025Article
- Bibliometric Analysis of Non-coding RNAs and Ischemic Stroke: Trends, Frontiers, and Challenges.Molecular biotechnology · 2025Review
- A20 negatively regulates necroptosis-induced microglia/macrophages polarization and mediates cerebral ischemic tolerance via inhibiting the ubiquitination of RIP3.Cell death & disease · 2024Article
- Mechanisms Behind the Impact of PIWI Proteins on Cancer Cells: Literature Review.International journal of molecular sciences · 2024Review
- Hypoxic postconditioning modulates neuroprotective glial reactivity in a 3D cortical ischemic-hypoxic injury model.Scientific reports · 2024Article
- The potential emerging role of piRNA/PIWI complex in virus infection.Virus genes · 2024Review
- Article
- Review
- Novel roles of PIWI proteins and PIWI-interacting RNAs in human health and diseases.Cell communication and signaling : CCS · 2023Review
- Attenuation of Piwil2 induced by hypoxic postconditioning prevents cerebral ischemic injury by inhibiting CREB2 promoter methylation.Brain pathology (Zurich, Switzerland) · 2023Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Epigenetic modification contributes to the pathogenesis of cerebral ischemia. Piwil2 belongs to the PIWI proteins subfamily and has a key role in the regulation of gene transcription through epigenetics. However, the roles of Piwil2 in cerebral ischemia have not been investigated. In this study, we aim to elucidate the roles and the underlying molecular mechanisms of Piwil2 in ischemic tolerance induced by hypoxic postconditioning (HPC) against transient global cerebral ischemia (tGCI). We found that the expression of Piwil2 in CA1 was downregulated by HPC after tGCI. Silencing Piwil2 with antisense oligodeoxynucleotide (AS-ODN) in CA1 after tGCI decreased the expression of apoptosis-related proteins and exerted neuroprotective effects. Opposite results were observed after overexpression of Piwil2 induced by administration of Piwil2-carried lentivirus. Furthermore, we revealed differentially expressed Piwil2-interacting piRNAs in CA1 between HPC and tGCI groups by RNA binding protein immunoprecipitation (RIP) assay. Moreover, downregulating Piwil2 induced by HPC or AS-ODN after tGCI caused a marked reduction of DNA methyltransferase 3A (DNMT3A), which in turn abolished the tGCI-induced increase in the DNA methylation of cyclic AMP response element-binding 2 (CREB2), thus increasing mRNA and protein of CREB2. Finally, downregulating Piwil2 restored dendritic complexity and length, prevented the loss of dentritic spines, thereby improving cognitive function after tGCI. These data firstly reveal that Piwil2 plays an important part in HPC-mediated neuroprotection against cerebral ischemia through epigenetic regulation of CREB2.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.