Evidence map›Paper›PMID 31217261›Full record

ArticleBioscience reports2019

PLCE1 promotes myocardial ischemia-reperfusion injury in H/R H9c2 cells and I/R rats by promoting inflammation.

WenHua Li, Yong Li, Ying Chu, WeiMin Wu, QiuHua Yu, XiaoBo Zhu, Qiang Wang

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. 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
1.5field-weighted citation impact, top 18% 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, 41 citations in OpenAlex.

  1. Review
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  15. TRPA1 as Target in Myocardial Infarction.International journal of molecular sciences · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. GSK3Oxidative medicine and cellular longevity · 2022
    Article
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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

7 authors.

WenHua LiDepartment of Cardiology, Wujin People's Hospital of Changzhou, Changzhou 213017, China.
Yong LiDepartment of Cardiology, Wujin People's Hospital of Changzhou, Changzhou 213017, China.
Ying ChuCentral Laboratory, Wujin People's Hospital of Changzhou, Changzhou 213017, China.
WeiMin WuDepartment of Cardio-Thoracic, Wujin People's Hospital of Changzhou, Changzhou 213017, China.
QiuHua YuDepartment of Cardio-Thoracic, Wujin People's Hospital of Changzhou, Changzhou 213017, China.
XiaoBo ZhuDepartment of Cardio-Thoracic, Wujin People's Hospital of Changzhou, Changzhou 213017, China.
Qiang WangDepartment of Cardio-Thoracic, Wujin People's Hospital of Changzhou, Changzhou 213017, China qiangwwujin@163.com.ORCID 0000-0001-7253-4747

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischemia-reperfusion (I/R) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. How to ensure the recovery of blood supply to ischemic myocardial tissue while avoiding or reducing I/R injury remains a critical problem in clinical practice. In the present study, we examined the function of phospholipase C ϵ-1 (PLCE1) by an H9c2 H/R (H/R, hypoxia-reoxygenation) model and a rat myocardial I/R injury model. The expression of PLCE1 and its effect on I/R injury-induced inflammatory response as well as its possible underlying mechanism were investigated. Our results have shown that PLCE1 was progressively increased along with the increase in hypoxia time in the H/R H9c2 and HL-1 cells. In myocardial I/R rats, PLCE1 presented a low expression level in the sham group, however, it was increased sharply in the I/R group. Overexpression of PLCE1 promoted the expression of IL-6, TNF-α, and IL-1α, and decreased the expression of IL-10. Knockdown of PLCE1 decreased the expression of IL-6, TNF-α, and IL-1α, and increased the expression of IL-10. Furthermore, overexpression of PLCE1 increased the phosphorylation of p38, ERK1/2, and nuclear factor-κ B (NF-κB) P65 while knockdown of PLCE1 inhibited their phosphorylation. In conclusion, the present study provided evidence that PLCE1 was up-regulated in H/R H9c2 cell and I/R rat. Overexpression of PLCE1 promoted the inflammatoion via activation of the NF-κB signaling pathway.

Indexed as

AnimalsCell LineGene Expression RegulationGene Knockdown TechniquesHumansInflammationInterleukin-10Interleukin-1alphaInterleukin-6MAP Kinase Signaling SystemMyocardial Ischemiap38 Mitogen-Activated Protein KinasesPhosphoinositide Phospholipase CPhosphorylationRatsReperfusion InjuryInterleukin-10Interleukin-1alphaInterleukin-6p38 Mitogen-Activated Protein KinasesPhosphoinositide Phospholipase Cphospholipase C epsilonTumor Necrosis Factor-alphaInflammationMyocardial ischemia-reperfusion injuryNF-κBPLCE1

Identifiers

PMID31217261
PMCPMC6609553
OpenAlexW2951459887

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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.