Evidence map›Paper›PMID 34786071›Full record

ArticleAmerican journal of translational research2021

miR-21-5p inhibits inflammation injuries in LPS-treated H9c2 cells by regulating PDCD4.

Jianhua Xue, Jiajia Liu, Bo Xu, Junbo Yu, Aixian Zhang, Lili Qin, Chun Liu, Yang Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 22% 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, 19 citations in OpenAlex.

  1. Article
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  7. The Ambivalent Role of miRNA-21 in Trauma and Acute Organ Injury.International journal of molecular sciences · 2024
    Review
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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 2 institutions in 1 country.

Jianhua XueDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Jiajia LiuDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Bo XuDepartment of Orthopaedics, Qidong Hospital of Traditional Chinese Medicine Nantong, Jiangsu Province, China.
Junbo YuDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Aixian ZhangDepartment of General Practice Medicine, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Lili QinDepartment of Endoscopic Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Chun LiuDepartment of Emergency Medicine, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Yang YangDepartment of Trauma Center, Affiliated Hospital of Nantong University Nantong, Jiangsu Province, China.
Nantong University · CNAnyang Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo explore the expression levels and the potential regulatory mechanism of miR-21-5p in LPS-treated H9c2 cells.

methodsThe secretions of the inflammatory cytokines induced by LPS in H9c2 cells were evaluated using ELISA. We used RT-RCR and western blot to measure the relative mRNA and protein expression levels in LPS-treated H9c2 cells. CCK-8 and EdU assays showed the viability and proliferation profiles of the H9c2 cells. TUNEL assays demonstrated the apoptotic behaviors of the H9c2 cells, and a luciferase reporter analysis was used to investigate the interactions between miR-21-5p and programmed cell death protein 4 (PDCD4).

resultsLPS induced damage to the H9c2 cells by reducing the cell viability and down-regulating miR-21-5p. On the other hand, miR-21-5p overexpression inhibited the LPS-induced inflammatory damage in the H9c2 cells. Moreover, PDCD4 was verified as a downstream target gene of miR-21-5p, and its expression was inhibited by the higher miR-21-5p content. Finally, miR-21-5p inhibited septic processes, and the PDCD4 overexpression rescued the miR-21-5p effect in the LPS-treated H9c2 cells.

conclusionOur findings suggest that miR-21-5p inhibits the LPS-induced progression of sepsis in H9c2 cells. Additionally, PDCD4 is a downstream target gene of miR-21-5p, and both molecules serve as potential therapeutic targets for heart sepsis patients.

Indexed as

H9c2 cellsheart sepsisLPSmiR-21-5pprogrammed cell death protein 4

Identifiers

PMID34786071
PMCPMC8581922
OpenAlexW3211574394

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.