Evidence map›Paper›PMID 32270599›Full record

ArticleJournal of cellular and molecular medicine2020

LINC00963 targeting miR-128-3p promotes acute kidney injury process by activating JAK2/STAT1 pathway.

Li-Bo Xie, Bo Chen, Xue Liao, Yi-Feng Chen, Rui Yang, Si-Rong He, Li-Jun Pei, Rui Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  16. LINC00963 May Be Associated with a Poor Prognosis in Patients with Cervical Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2022
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4 · The record

Corrections and comments

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

8 authors at 3 institutions in 1 country.

Li-Bo XieDepartment of Urology, Nephropathy Clinical Medical Research Center of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Bo ChenDepartment of Human Anatomy, School of Basic Medical Sciences, Southwest Medical University, Luzhou, China.
Xue LiaoCollege of Clinical Medicine, Southwest Medical University School of Clinical Medical Sciences, Luzhou, China.
Yi-Feng ChenCollege of Clinical Medicine, Southwest Medical University School of Clinical Medical Sciences, Luzhou, China.
Rui YangCollege of Clinical Medicine, Southwest Medical University School of Clinical Medical Sciences, Luzhou, China.
Si-Rong HeDepartment of Immunology, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China.
Li-Jun PeiDepartment of Urology, Nephropathy Clinical Medical Research Center of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Rui JiangDepartment of Urology, Nephropathy Clinical Medical Research Center of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, China.ORCID 0000-0003-1849-3643
Southwest Medical University · CNAffiliated Hospital of Southwest Medical University · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of long non-coding RNAs (lncRNAs) in kidney diseases has been gradually discovered in recent years. LINC00963, as an lncRNA, was found to be involved in chronic renal failure. However, the role and molecular mechanisms of LINC00963 engaged in acute kidney injury (AKI) were still unclear. In this study, we established rat AKI models by ischaemia and reperfusion (I/R) treatment. Urea and creatinine levels were determined, and histological features of kidney tissues were examined following HE staining. CCK8 assay was chosen to assess the viability of hypoxia-induced HK-2 cells. Dual-luciferase reporter gene assays were performed to verify the target relationship between LINC00963 and microRNA. The mRNA and protein levels were assayed by RT-qPCR and Western blot, respectively. Annexin V-FITC/PI and TUNEL staining were used to evaluate apoptosis. LINC00963 was highly expressed in the cell and rat models, and miR-128-3p was predicted and then verified as a target gene of LINC00963. Knockdown of LINC00963 reduced acute renal injury both in vitro and in vivo. LINC00963 activated the JAK2/STAT1 pathway to aggravate renal I/R injury. LINC00963 could target miR-128-3p to reduce G1 arrest and apoptosis through JAK2/STAT1 pathway to promote the progression of AKI.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCell LineGene Knockout TechniquesJanus Kinase 2MaleMicroRNAsRatsRNA, Long NoncodingSTAT1 Transcription FactorJak2 protein, ratJanus Kinase 2long non-coding RNA LINC00963, humanMicroRNAsMIRN128 microRNA, ratRNA, Long NoncodingStat1 protein, ratSTAT1 Transcription Factoracute kidney injuryapoptosisLINC00963miR-128-3pSTAT1 pathway

Identifiers

PMID32270599
PMCPMC7214170
OpenAlexW3015702218

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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.