Evidence map›Paper›PMID 26757107›Full record

ArticleJournal of cellular and molecular medicine2016

Progranulin deficiency leads to severe inflammation, lung injury and cell death in a mouse model of endotoxic shock.

Yuan Yu, Xiaoying Xu, Lu Liu, Sheng Mao, Tingting Feng, Yi Lu, Yizhe Cheng, Hongyan Wang, Weiming Zhao, Wei Tang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  16. Article
  17. Progranulin deficiency in Iba-1Journal of neuroinflammation · 2021
    Article
  18. 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

10 authors at 4 institutions in 1 country.

Yuan YuDepartment of Hematology, Qilu Hospital, Shandong University, Jinan, Shandong, China.
Xiaoying XuDepartment of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Lu LiuDepartment of Pathology, Huai'an First People's Hospital, Huai'an, Jiangsu, China.
Sheng MaoDepartment of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Tingting FengDepartment of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Yi LuDepartment of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Yizhe ChengDepartment of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Hongyan WangDepartment of Medical Microbiology, Weifang Medical University, Weifang, Shandong, China.
Weiming ZhaoDepartment of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Wei TangDepartment of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, China.
Shandong University · CNHuaian First People’s Hospital · CNQilu Hospital of Shandong University · CNWeifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progranulin (PGRN) is a crucial secreted growth factor involved in various kinds of physiologic and disease processes and often has a protective role in inflammatory diseases. This study was designed to investigate the protective effects of PGRN on endotoxic shock in a mouse model of PGRN deficiency. After lipopolysaccharide (LPS) injection to induce endotoxic shock in mice, PGRN levels were induced in wild-type (WT) mice at 6 and 24 hrs. Survival rate analysis, haematoxylin and eosin staining, immunohistochemical staining, enzyme-linked immunosorbent assay and in situ terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick-end labelling assay were used to reveal the susceptibility, lung injury, inflammatory cell infiltration, production of inflammatory mediators and lung cell death in mice after LPS injection. PGRN-deficient (Grn(-/-) ) mice were highly susceptible to LPS-induced endotoxic shock, with decreased survival, severe lung injury, increased production of pro-inflammatory mediators, and inflammatory cell infiltration and apoptotic death in the lung. Additionally, recombinant PGRN (rPGRN) administration before LPS stimulation ameliorated the survival of and abnormalities in both WT and Grn(-/-) mice. Altogether, these findings indicate that PGRN may be a novel biologic agent with therapeutic potential for endotoxic shock probably by inhibiting LPS-induced systemic and local inflammation in mice for treating endotoxic shock.

Indexed as

AnimalsApoptosisCytokinesGranulinsInflammationIntercellular Signaling Peptides and ProteinsLipopolysaccharidesLung InjuryMacrophagesMaleMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationProgranulinsShock, SepticCytokinesGranulinsGrn protein, mouseIntercellular Signaling Peptides and ProteinsLipopolysaccharidesProgranulinsendotoxic shockinflammationlipopolysaccharideprogranulin

Identifiers

PMID26757107
PMCPMC4759474
OpenAlexW2232615600

What OpenQuestion holds

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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.