Evidence map›Paper›PMID 32794050›Full record

ArticleInflammation2020

LncRNA KCNQ1OT1 Regulates Endoplasmic Reticulum Stress to Affect Cerebral Ischemia-Reperfusion Injury Through Targeting miR-30b/GRP78.

Yue Li, Ming Yi, Dan Wang, Qiuxia Zhang, Li Yang, Chunsheng Yang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 13% of its field
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

14 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Yue Li *Department of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Ming Yi *Department of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Dan WangDepartment of Clinical Laboratory, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
Qiuxia ZhangDepartment of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Li YangDepartment of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China.
Chunsheng YangDepartment of Neurology, Tianjin Medical University General Hospital, 154 AnShan road, HePing District, Tianjin, 300052, China. chunshengyang@163.com.ORCID http://orcid.org/0000-0002-3847-9526
Tianjin Medical University General Hospital · CNFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China 81571172
6 · The paper itself

Abstract

Endoplasmic reticulum stress (ERS) plays an important role in cerebral ischemia-reperfusion injury (CIRI) by regulating apoptosis. Although the role of long non-coding RNA (LncRNA) KCNQ1OT1 in CIRI has been reported, the specific mechanism is still unclear. In this paper, the regulation of ERS by LncRNA KCNQ1OT1 in CIRI and its mechanism were studied. Transient middle cerebral artery occlusion (tMCAO) model was established in SD rats with KCNQ1OT1 intervention. PC12 cells were used to construct the OGD/R cell model. The expressions of LncRNA KCNQ1OT1 and miR-30b were detected by RT-qPCR. TCC staining was used to detect the extent of cerebral ischemia. TUNEL staining was used to detect apoptosis level, and Western blot was used to detect the expressions of ERS and apoptosis-related proteins. The targeted binding of LncRNA KCNQ1OT1, miR-30b, and GRP78 was detected by double luciferase assay. The expressions of LncRNA KCNQ1OT1 and miR-30b were interfered by cell transfection. Cell proliferation was detected by CCK-8. The level of LncRNA KCNQ1OT1 was increased and that of miR-30b was decreased in the blood samples of patients with CIRI. In tMCAO rats with KCNQ1OT1 intervention, the expression of miR-30b was increased, and the ischemic range of brain tissues was decreased. What's more, the level of ERS was decreased, and the apoptosis of brain tissues was decreased. LncRNA KCNQ1OT1 could regulate miR-30b/GRP78 in OGD/R cells in a targeted way. Intervention of KCNQ1OT1 could promote the proliferation of OGD/R cells, inhibiting the level of ERS and cell apoptosis. Further inhibition of miR-30b could reverse the effect of intervention of KCNQ1OT1. LncRNA KCNQ1OT1 regulates ERS to affect CIRI through targeting miR-30b/GRP78.

Indexed as

Endoplasmic Reticulum StressRNA, Long NoncodingAnimalsApoptosisBrainBrain IschemiaCell ProliferationEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHumansInfarction, Middle Cerebral ArteryMicroRNAsNeuronsPC12 CellsProtein BindingRatsEndoplasmic Reticulum Chaperone BiPGRP78 protein, ratHeat-Shock ProteinsHSPA5 protein, humanKCNQ1OT1 RNAMicroRNAsMIRN30 microRNA, ratRNA, Long Noncodingcerebral ischemia-reperfusion injuryendoplasmic reticulum stressGRP78LncRNA KCNQ1OT1miR-30b

Identifiers

PMID32794050
OpenAlexW3049381251

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.