Evidence map›Paper›PMID 25888255›Full record

ArticleCritical care (London, England)2015

An ADAM10 promoter polymorphism is a functional variant in severe sepsis patients and confers susceptibility to the development of sepsis.

Lili Cui, Yan Gao, Yuliu Xie, Yan Wang, Yujie Cai, Xin Shao, Xiaotang Ma, You Li, Guoda Ma, Gen Liu and 9 more

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. ADAM10-a "multitasker" in sepsis: focus on its posttranslational target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. TheScience translational medicine · 2019
    Article
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  20. Review
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

19 authors at 2 institutions in 1 country.

Lili CuiGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. lilicui1983@aliyun.com.
Yan GaoThe Intensive Care Unit, the Forth Affiliated Hospital of Harbin Medical University, Harbin, China. gaoyan_1971@126.com.
Yuliu XieThe Intensive Care Unit, Affiliated Hospital of Guangdong Medical College, Zhanjiang, PR China. sasa711711@qq.com.
Yan WangClinical Research Center of Guangdong Medical College, Affiliated Hospital of Guangdong Medical College, Zhanjiang, PR China. jojoyan@aliyun.com.
Yujie CaiGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. 434775643@qq.com.
Xin ShaoThe Intensive Care Unit, Affiliated Hospital of Guangdong Medical College, Zhanjiang, PR China. 812672728@qq.com.
Xiaotang MaGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. mxtgdmc@163.com.
You LiGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. dreamerly2001@163.com.
Guoda MaGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. maguoda@gdmc.edu.cn.
Gen LiuGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. 363816619@qq.com.
Wanwen ChengGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. 619448969@qq.com.
Yu LiuGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. 353360830@qq.com.
Tingting LiuGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. 563876302@qq.com.
Qunwen PanGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. pqwforeve@163.com.
Hua TaoGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. taohua1943@126.com.
Zhou LiuGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. liuzhou102@126.com.
Bin ZhaoGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. zhaobine@vip.tom.com.
Yiming ShaoThe Intensive Care Unit, Affiliated Hospital of Guangdong Medical College, Zhanjiang, PR China. yimingshao_gmc@126.com.
Keshen LiGuangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Affiliated Hospital of Guangdong Medical College, Renmin street south 57, Xiashan district, Zhanjiang City, 524001, Guangdong Province, PR China. keshenli1971@126.com.
Guangdong Medical College · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAlthough genetic variants of the A disintegrin and metalloproteinase 10 (ADAM10) gene have been shown to be associated with susceptibility to several inflammatory-related diseases, to date little is known about the clinical relationship in the development of sepsis.

methodsTwo genetic variants in the promoter of ADAM10 were selected to analyze the potential association with the risk of sepsis. A total of 440 sepsis patients and 450 matched healthy individuals in two independent Chinese Han population were enrolled. Pyrosequencing and polymerase chain reaction-length polymorphism was used to determine the genotypes of the rs514049 and rs653765. A real-time qPCR method was used to detect the mRNA level of ADAM10. Enzyme-linked immunosorbent assay was used to measure the expression levels of substrates CX3CL1, interleukin (IL)-6R, tumor necrosis factor alpha (TNF-α), and the pro-inflammatory cytokines IL-1β and IL-6. Luciferase assay was used to analyze the activities of the promoter haplotypes of ADAM10.

resultsNo statistically significant differences between sepsis cases and controls in the genotype or allele frequencies were observed, suggesting that ADAM10 single nucleotide polymorphisms (SNPs) may not be risk factors for the occurrence of sepsis. A significant difference in the genotype and allele frequencies of the rs653765 SNP between patients with sepsis subtype and severe sepsis (P = 0.0014) or severe sepsis/sepsis shock (P = 0.0037) were observed. Moreover, the rs653765 CC genotype in severe sepsis showed a higher ADAM10 level compared to healthy groups, and the rs653765 CC polymorphism had a strong impact on the production of the ADAM10 substrates CX3CL1, IL-6R and TNF-α. Furthermore, the functional assay showed that ADAM10 C-A haplotype carriers exhibited significantly higher reporter activity compared with the T-A carriers and T-C carriers in human acute monocytic leukemia cell line.

conclusionsOur data initially indicated the ADAM10 rs653765 polymorphism was associated with the development of severe sepsis; the risk CC genotype could functionally affect the expression level of ADAM10 mRNA and was accompanied by the up-regulation of its substrates. Thus, ADAM10 might be clinically important and play a critical role in the pathogenesis of the development of sepsis, with potentially important therapeutic implications.

Indexed as

Polymorphism, Single NucleotideADAM10 ProteinADAM ProteinsAdultAgedAged, 80 and overAmyloid Precursor Protein SecretasesAsian PeopleCase-Control StudiesChinaCytokinesFemaleGene FrequencyHaplotypesHumansInterleukinsADAM10 ProteinADAM10 protein, humanADAM ProteinsAmyloid Precursor Protein SecretasesCytokinesInterleukinsMembrane Proteins

Identifiers

PMID25888255
PMCPMC4373036
OpenAlexW2121565761

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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.