Evidence map›Paper›PMID 31900829›Full record

ArticleInflammation2020

lncRNA RMRP Prevents Mitochondrial Dysfunction and Cardiomyocyte Apoptosis via the miR-1-5p/hsp70 Axis in LPS-Induced Sepsis Mice.

Ying Han, Yixin Cai, Xiaoquan Lai, Zhenling Wang, Shiqing Wei, Kun Tan, Min Xu, Hongyan Xie

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 3 pooled it
5.6field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 3 syntheses or guidelines pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  3. MicroRNAs and Sepsis-Induced Cardiac Dysfunction: A Systematic Review.International journal of molecular sciences · 2020
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  13. Current Perspectives of Mitochondria in Sepsis-Induced Cardiomyopathy.International journal of molecular sciences · 2024
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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.

Ying HanDepartment of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Yixin CaiDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. yixincai02@163.com.
Xiaoquan LaiDepartment of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Zhenling WangDepartment of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Shiqing WeiDepartment of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Kun TanDepartment of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Min XuDepartment of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Hongyan XieDepartment of Hospital Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Tongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both long non-coding RNA (lncRNA) RMRP and heat shock protein (HSP) 70 have been known to play crucial roles in inflammation. The present study investigated the roles of lncRNA RMRP and HSP70 protein 4 (HSPA4) in lipopolysaccharide (LPS)-induced sepsis. The C57BL/6 mice were treated with LPS, following which the cardiomyocytes were isolated for in vitro experiments. Further, a cardiac muscle cell line, HL-1 was transfected with plasmids expressing RMRP and HSPA4, si-NC, si-HSPA4, miR-1-5p mimic, and controls in vitro. Cell apoptosis, mitochondrial membrane potential (MMP), and levels of intracellular reactive oxygen species (ROS), mRNAs, and proteins were detected in the transfected mice tissues and cells. The LPS treatment significantly reduced the expression levels of RMRP, MMP, and mitochondrial cytochrome C. Moreover, it enhanced the cardiomyocyte apoptosis, intracellular ROS levels, cytoplasm cytochrome C levels, and the expression of caspase-3 and caspase-9 and nuclear factor κB (NF-κB) p65 subunit. The predicted RMRP-miR-1-5p-HSPA4 network was validated by co-transfection experiments in vitro in HL-1 cells. The transfection of miR-1-5p-treated cells with pcDNA-RMRP enhanced the levels of the protein HSPA4; however, no change at the mRNA level was observed. Moreover, miR-1-5p mimic attenuated the protective effect of pcDNA-HSPA4 against LPS-induced mitochondrial damage and apoptosis. In addition, we observed that silencing of HSPA4 increased the expression of nuclear p65; however, this effect could be reversed by co-transfection with pcDNA-RMRP. The lncRNA RMRP axis acts as a sponge for miR-1-5p. RMRP inhibits LPS-induced apoptosis of cardiomyocytes and mitochondrial damage by suppressing the post-transcriptional regulatory function of miR-1-5p on HSPA4. We believe that RMRP exhibits therapeutic potential for LPS-induced myocardial dysfunction both in vitro and in vivo.

Indexed as

AnimalsApoptosisCells, CulturedHSP70 Heat-Shock ProteinsLipopolysaccharidesMaleMiceMice, Inbred C57BLMicroRNAsMitochondriaMyocytes, CardiacRNA, Long NoncodingSepsisHSP70 Heat-Shock ProteinsLipopolysaccharidesMicroRNAsMirn1 microRNA, mouseRMRP non-coding RNA, humanRNA, Long NoncodingcardiomyocyteHSPA4lncRNA RMRPmiR-1-5psepsis

Identifiers

PMID31900829
OpenAlexW2996855416

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.