Evidence map›Paper›PMID 34351574›Full record

ArticleMolecular and cellular biochemistry2021

MicroRNA-197-3p mediates damage to human coronary artery endothelial cells via targeting TIMP3 in Kawasaki disease.

Chaowu Liu, Deguang Yang, Hong Wang, Shengwei Hu, Xiaofei Xie, Li Zhang, Hongling Jia, Qi Qi

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
1.9field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 2 syntheses or guidelines pooled it, 12 citations in OpenAlex.

  1. Pooled it
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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.

Chaowu Liu *Institute of Mass Spectrometer and Atmospheric Environment, Jinan University, Guangzhou, 510632, China.
Deguang Yang *Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China.
Hong Wang *Guangdong Province Engineering Research Center for Antibody Drug and Immunoassay, Colleges of Life Science and Technology, Jinan University, Guangzhou, 510632, Guangdong, China.
Shengwei HuMOE Key Laboratory of Tumor Molecular Biology, Clinical Translational Center for Targeted Drug, Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China.
Xiaofei XieDepartment of Pediatric Cardiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, Guangdong, China.
Li ZhangDepartment of Pediatric Cardiology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, Guangdong, China.
Hongling JiaDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China. jiahongling@aliyun.com.
Qi QiMOE Key Laboratory of Tumor Molecular Biology, Clinical Translational Center for Targeted Drug, Department of Pharmacology, School of Medicine, Jinan University, Guangzhou, 510632, Guangdong, China. qiqikc@jnu.edu.cn.ORCID http://orcid.org/0000-0003-4460-0713
Jinan University · CNGuangzhou Medical University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 81973341
6 · The paper itself

Abstract

Kawasaki disease (KD) causes cardiovascular system injury in children. However, the pathogenic mechanisms of KD have not been well defined. Recently, strong correlation between aberrant microRNAs and KD nosogenesis has been revealed. A role of microRNA-197-3p (miR-197-3p) in the pathogenesis of KD is identified in the present study. Cell proliferation assay showed human coronary artery endothelial cells (HCAECs) were suppressed by serum from KD patients, which was correlated with high levels of miR-197-3p in both KD serum and HCAECs cultured with KD serum. The inhibition of HCAECs by miR-197-3p was confirmed by cells expressing miR-197-3p mimic and miR-197-3p inhibitor. Comparative proteomics analysis and Ingenuity Pathway Analysis (IPA) revealed TIMP3 as a potential target of miR-197-3p, which was demonstrated by western blot and dual-luciferase reporter assays. Subsequently, by detecting the endothelium damage markers THBS1, VWF, and HSPG2, the role of miR-197-3p/TIMP3 in KD-induced damage to HCAECs was confirmed, which was further validated by a KD mouse model in vivo. The expressions of miR-197-3p and its target, TIMP3, are dramatically variational in KD serum and HCAECs cultured with KD serum. Increased miR-197-3p induces HCAECs abnormal by restraining TIMP3 expression directly. Hence, dysregulation of miR-197-3p/TIMP3 expression in HCAECs may be an important mechanism in cardiovascular endothelium injury in KD patients, which offers a feasible therapeutic target for KD treatment.

Indexed as

AnimalsApoptosisCells, CulturedChild, PreschoolCoronary Artery DiseaseEndothelial CellsFemaleHumansInfantMaleMiceMice, Inbred C57BLMicroRNAsMucocutaneous Lymph Node SyndromeProteomeTissue Inhibitor of Metalloproteinase-3MicroRNAsMIRN197 microRNA, humanProteomeTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3Human coronary artery endothelial cellsKawasaki diseasemiR-197-3pTIMP3

Identifiers

PMID34351574
OpenAlexW3192313988

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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.