Evidence map›Paper›PMID 27844279›Full record

ArticleMolecular neurobiology2017

LncRNA-N1LR Enhances Neuroprotection Against Ischemic Stroke Probably by Inhibiting p53 Phosphorylation.

Zhuomin Wu, Ping Wu, Xialin Zuo, Na Yu, Yixin Qin, Qian Xu, Shuai He, Bohong Cen, Wenjie Liao, Aimin Ji

Erratum issuedAbstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing 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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

67 citing papers in PubMed.

  1. Review
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  8. Ferroptosis inhibitors: past, present and future.Frontiers in pharmacology · 2024
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  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Long Non-coding RNAs (lncRNAs), A New Target in Stroke.Cellular and molecular neurobiology · 2022
    Review
  19. Article
  20. Article

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Zhuomin WuCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Industrial avenue253, Guangzhou, 510282, China.
Ping WuPharmacy Department, Chengdu First People's Hospital/ Chengdu Integrated TCM & Western Medicine Hospital, Chengdu, China.
Xialin ZuoInstitute of Neurosciences and the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Na YuThe Second Clinical College of Southern Medical University, Guangzhou, China.
Yixin QinCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Industrial avenue253, Guangzhou, 510282, China.
Qian XuCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Industrial avenue253, Guangzhou, 510282, China.
Shuai HeCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Industrial avenue253, Guangzhou, 510282, China.
Bohong CenCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Industrial avenue253, Guangzhou, 510282, China.
Wenjie LiaoCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Industrial avenue253, Guangzhou, 510282, China.
Aimin JiCenter for Drug Research and Development, Zhujiang Hospital, Southern Medical University, Industrial avenue253, Guangzhou, 510282, China. aiminji_007@163.com.

Funding

the National Nature Science Foundation of China NSFC81370449
6 · The paper itself

Abstract

In recent years, long noncoding RNAs (lncRNAs) have been shown to have critical roles in a broad range of cell biological processes. However, the activities of lncRNAs during ischemic stroke remain largely unknown. In this study, we carried out a genome-wide lncRNA microarray analysis in rat brains with ischemia/reperfusion (I/R) injury. The results revealed the differential expression of a subset of lncRNAs. Through the construction of lncRNA-mRNA co-expression networks, we identified lncRNA-N1LR as a novel I/R-induced lncRNA. The functions of lncRNA-N1LR were assessed by silencing and overexpressing this lncRNA in vitro and in vivo. We found that lncRNA-N1LR enhanced cell cycle progression and cell proliferation, and inhibited apoptosis in N2a cells subjected to in vitro ischemia (oxygen-glucose deprivation/reoxygenation, OGD/R). Furthermore, we showed that lncRNA-N1LR reduced neuronal apoptosis and neural cell loss in I/R-induced mouse brains. Mechanistically, we discovered that lncRNA-N1LR promoted neuroprotection probably through the inhibition of p53 phosphorylation on serine 15 in a manner that was independent of its location-associated gene Nck1. In summary, our results indicated that lncRNA-N1LR promoted neuroprotection against ischemic stroke probably by inactivating p53. Thus, we propose that lncRNA-N1LR may serve as a potential target for therapeutic intervention following ischemic brain injury.

Indexed as

AnimalsBase SequenceBrain IschemiaMaleMiceMice, Inbred C57BLNeuroprotectionPhosphorylationRatsRats, Sprague-DawleyRNA, Long NoncodingStrokeTumor Suppressor Protein p53RNA, Long NoncodingTumor Suppressor Protein p53ApoptosisCell proliferationIschemic strokelncRNA-N1LRNeuroprotectionp53

Identifiers

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Registered trials

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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.