Evidence map›Paper›PMID 31231384›Full record

ArticleFrontiers in immunology2019

PRAK Is Required for the Formation of Neutrophil Extracellular Traps.

Yan Wang, Yuqing Wang, Jia Wu, Chen Liu, Yu Zhou, Ligu Mi, Yu Zhang, Wei Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 15 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

8 authors at 3 institutions in 1 country.

Yan WangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, China.
Yuqing WangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, China.
Jia WuDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, China.
Chen LiuDepartment of Clinical Laboratory, Peking University People's Hospital, Beijing, China.
Yu ZhouDepartment of Pharmacology, Institute of Materia Medica, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Ligu MiDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, China.
Yu ZhangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, China.
Wei WangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, China.
Peking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophil extracellular traps (NETs) are one of the most powerful and specific tools for neutrophils to clean up extracellular microbes, but the mechanisms of NETosis under infection are scarcely studied. In this study, by examining the neutrophils from human peripheral blood and mouse abdomen, we demonstrated that PRAK dysfunction resulted in a significantly reduced NET formation and elevated apoptotic cells. Furthermore, PRAK dysfunction could lead to impaired NET-mediated antibacterial activity and shorten the survival of mice with CLP-induced sepsis. Mechanism studies revealed that attenuated NET formation in PRAK dysfunctional neutrophils correlated with overproduction of reactive oxygen species (ROS), which triggered apoptosis through excessive autophagy. The imbalance of NET formation and apoptosis was further regulated by treatment with lower ROS in hypoxia. Here, we propose a novel candidate, PRAK, which can sense the oxidative stress and regulate the releasing of ROS, may be the master molecular switch to regulate the NETosis-apoptosis axis of neutrophils.

Indexed as

AnimalsApoptosisAutophagyBacteriaCaspase 3CytokinesDisease Models, AnimalExtracellular TrapsHumansIntracellular Signaling Peptides and ProteinsMiceNeutrophilsOxidative StressPhagocytosisProtein Serine-Threonine KinasesReactive Oxygen SpeciesCaspase 3CytokinesIntracellular Signaling Peptides and ProteinsMAP-kinase-activated kinase 5Protein Serine-Threonine KinasesReactive Oxygen Speciesapoptosisautophagyneutrophil extracellular traps (NETs)PRAKreactive oxygen species (ROS)

Identifiers

PMID31231384
PMCPMC6559312
OpenAlexW3140945558

What OpenQuestion holds

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LicenceCC BY
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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.