Evidence map›Paper›PMID 26659076›Full record

ArticleApoptosis : an international journal on programmed cell death2016

SOX6 and PDCD4 enhance cardiomyocyte apoptosis through LPS-induced miR-499 inhibition.

Zhuqing Jia, Jiaji Wang, Qiong Shi, Siyu Liu, Weiping Wang, Yuyao Tian, Qin Lu, Ping Chen, Kangtao Ma, Chunyan Zhou

Open access · hybridAbstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 11% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Zhuqing JiaDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China.
Jiaji WangBeijing Jianhua Experimental School, Yuquan Road 66, Haidian District, Beijing, China.
Qiong ShiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China.
Siyu LiuDepartment of Epidemiology, Rollins School of Public Health, Emory University, 1518 Clifton Road NE, Atlanta, GA, 30322, USA.
Weiping WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China.
Yuyao TianDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China.
Qin LuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China.
Ping ChenDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China.
Kangtao MaDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China.
Chunyan ZhouDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, No. 38, Xueyuan Road, Haidian District, Beijing, China. chunyanzhou@bjmu.edu.cn.
Peking University · CNBeijing Haidian Hospital · CNEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-induced cardiac apoptosis is one of the major pathogenic factors in myocardial dysfunction. As it enhances numerous proinflammatory factors, lipopolysaccharide (LPS) is considered the principal mediator in this pathological process. However, the detailed mechanisms involved are unclear. In this study, we attempted to explore the mechanisms involved in LPS-induced cardiomyocyte apoptosis. We found that LPS stimulation inhibited microRNA (miR)-499 expression and thereby upregulated the expression of SOX6 and PDCD4 in neonatal rat cardiomyocytes. We demonstrate that SOX6 and PDCD4 are target genes of miR-499, and they enhance LPS-induced cardiomyocyte apoptosis by activating the BCL-2 family pathway. The apoptosis process enhanced by overexpression of SOX6 or PDCD4, was rescued by the cardiac-abundant miR-499. Overexpression of miR-499 protected the cardiomyocytes against LPS-induced apoptosis. In brief, our results demonstrate the existence of a miR-499-SOX6/PDCD4-BCL-2 family pathway in cardiomyocytes in response to LPS stimulation.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCells, CulturedHeart VentriclesHeLa CellsHumansLipopolysaccharidesMicroRNAsMyocytes, CardiacRats, Sprague-DawleyRNA InterferenceSOXD Transcription FactorsApoptosis Regulatory ProteinsLipopolysaccharidesMicroRNAsMIRN499 microRNA, ratPdcd4 protein, ratSOXD Transcription FactorsApoptosisCardiomyocyteLPSmiR-499PDCD4SOX6

Identifiers

PMID26659076
PMCPMC4712245
OpenAlexW2289162037

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.