Evidence map›Paper›PMID 39996480›Full record

ArticleCNS neuroscience & therapeutics2025

Hypoxic Postconditioning Offers Neuroprotection Against Transient Cerebral Ischemia via Down-Regulation of rno_piR_011022.

Meiyan Chen, Shanshan Duan, Guorong Chai, Lixuan Zhan, Linhui Peng, Weiwen Sun, En Xu

Abstract read
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Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Meiyan ChenDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Shanshan DuanDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Guorong ChaiDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Lixuan ZhanDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Linhui PengDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Weiwen SunDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
En XuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.ORCID 0000-0001-7342-0047

Funding

the National Natural Science Foundation of China 81873745the National Natural Science Foundation of China 82071281the National Natural Science Foundation of China 82471309
6 · The paper itself

Abstract

backgroundPiwi-interacting RNAs (piRNAs) are differentially expressed after cerebral ischemia. However, little is known about their roles in transient global cerebral ischemia (tGCI). Herein, we aim to elucidate the roles and the underlying molecular mechanisms of piRNAs in tGCI and cerebral ischemic tolerance induced by hypoxic postconditioning (HPC).

methodsThe male rat models of tGCI and HPC were established in vivo. Oxygen-glucose deprivation/reoxygenation (OGD/R) was developed from primary hippocampal neurons in vitro. RNA-sequencing, fluorescence in situ hybridization, and quantitative real-time PCR were used for detecting piRNA expression. Immunohistochemistry, TUNEL staining, CCK8 assay, etc., were used to evaluate neuronal damage. Western blot was used to measure protein levels of NR2B, PSD95, and cleaved-caspase 3.

resultsThe expression profiles of piRNAs in CA1 were significantly changed after tGCI. HPC downregulated the expression of the top 5 piRNAs associated with synaptic function. Notably, the knockdown of rno_piR_011022 not only alleviated neuronal apoptosis and enhanced synaptic plasticity after tGCI and OGD/R but also reduced methyl-D-aspartate (NMDA) receptor 2B (NR2B) expression and inhibited NR2B-postsynaptic density 95 (PSD95) interaction following tGCI. HPC enhanced these inhibitory effects.

conclusionThis innovative study indicated that the down-regulation of rno_piR_011022 plays an important role in HPC-mediated neuroprotection against tGCI through inhibiting the NR2B-PSD95 interaction.

Indexed as

Ischemic Attack, TransientIschemic PostconditioningNeuroprotectionRNA, Small InterferingAnimalsCells, CulturedDown-RegulationHippocampusMaleNeuronsRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateReceptors, N-Methyl-D-AspartateRNA, Small Interferingapoptosiscerebral ischemiaNR2B‐PSD95rno_piR_011022synaptic plasticity

Identifiers

PMID39996480
PMCPMC11851155

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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.