Evidence map›Paper›PMID 31933818›Full record

ArticleInternational journal of clinical and experimental pathology2019

MiR-197-3p regulates endothelial cell proliferation and migration by targeting IGF1R and BCL2 in Kawasaki disease.

Yan Li, Xindan Wu, Fang Gao, Xianmin Wang

Open access · greenAbstract read
PubMed Full text at PMC
In one paragraph

Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Microrna Expression inMicroRNA (Shariqah, United Arab Emirates) · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Epigenetics in Kawasaki Disease.Frontiers in pediatrics · 2021
    Review
  12. Article
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

4 authors at 1 institution in 1 country.

Yan LiDepartment of Pediatric Cardiology, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China Chengdu 611731, China.
Xindan WuDepartment of Pediatric Cardiology, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China Chengdu 611731, China.
Fang GaoDepartment of Pediatric Cardiology, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China Chengdu 611731, China.
Xianmin WangDepartment of Pediatric Cardiology, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China Chengdu 611731, China.
Chengdu Women's and Children's Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKawasaki disease (KD) is a multisystemic vasculitis syndrome. Accumulating evidences indicated that microRNAs play a critical role in KD. However, the mechanism was still not fully understood. The study aimed to research the functions of microRNA-197-3p (miR-197-3p) in the progression of KD.

methodsLevel of miR-197-3p was detected by quantitative polymerase chain reaction (qRT-PCR) in acute KD serum. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to determine cell proliferation in HCAECs. Cell apoptosis was evaluated by flow cytometry. In addition, transwell assay was used to identify the migration capacity of HCAECs

resultsLevel of miR-197-3p was higher in Acute KD samples than that of healthy control and convalescent KD samples. Mechanistically, the role of miR-197-3p was exerted through directly targeting IGF1R and BCL2 in KD serum-induced HCAECs. Functionally, the inhibiting effect on cell apoptosis as well as promoting effects on cell proliferation and migration of miR-197-3p deletion was abrogated by either si-IGF1R or si-BCL2.

conclusionmiR-197-3p modifies cell behaviors of proliferation, apoptosis and migration by targeting IGF1R and BCL2 in KD, providing a new perspective for the treatment of KD clinically.

Indexed as

apoptosisBCL2IGF1RKDmigrationmiR-197-3pproliferation

Identifiers

PMID31933818
PMCPMC6949791
OpenAlexW3005450534

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.