Evidence map›Paper›PMID 32503416›Full record

ArticleBMC immunology2020

Progranulin inhibits LPS-induced macrophage M1 polarization via NF-кB and MAPK pathways.

Lianlian Liu, Hongmei Guo, Aimei Song, Jiahui Huang, Yu Zhang, Shanshan Jin, Shutong Li, Liguo Zhang, Chengzhe Yang, Pishan Yang

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 1 pooled it
20.4field-weighted citation impact, top 1% 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

135 citing papers in PubMed, 1 synthesis or guideline pooled it, 277 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. MPRO3 Regulates Macrophage Polarization and OsteoclastogenesisJournal of microbiology and biotechnology · 2026
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  12. Regulation of microglial activation by progranulin through the NF-κB pathway in subarachnoid hemorrhage and its effect on white matter injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  17. Upregulation of Parathyroid Hormone Receptor 1 (International journal of molecular sciences · 2026
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  20. Article

75 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Lianlian LiuDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Hongmei GuoDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Aimei SongDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Jiahui HuangDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Yu ZhangDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Shanshan JinDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Shutong LiDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Liguo ZhangDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China.
Chengzhe YangDepartment of Oral and Maxillofacial Surgery, Qilu Hospital and Institute of Stomatology, Shandong University, Jinan, 250012, Shandong, People's Republic of China. yangchengzhe19@163.com.
Pishan YangDepartment of Periodontology, School of Stomatology, Shandong University, 44 West Wenhua Road, Jinan, 250012, Shandong, People's Republic of China. yangps@sdu.edu.cn.
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

National Natural Science Foundation of China 81702684National Natural Science Foundation of China 81771076
6 · The paper itself

Abstract

backgroundMacrophage M1 polarization plays a pivotal role in inflammatory diseases. Progranulin (PGRN) has potential anti-inflammation action, however, the effect of PGRN on macrophage M1 polarization has been poorly studied. Our study aimed to investigate the effect of PGRN on lipopolysaccharide (LPS)-induced macrophage M1 polarization and clarify the underlying mechanisms.

methodsRAW264.7 cells were polarized to M1 macrophage by LPS with or without recombinant PGRN (rPGRN) and tumor necrosis factor alpha antibody (anti-TNF-α). A cell counting kit-8 assay (CCK-8), flow cytometry, Quantitative Real-Time PCR assay (q-PCR), Western blot assay and enzyme-linked immunosorbent assay (ELISA) were used to determine the effect of different treatments on cell proliferation, expression of surface phenotype marker and expressions and secretion of inflammatory cytokines. The activation of NF-κB/mitogen-activated protein kinase (MAPK) pathways and the nuclear translocation of NF-κB p65 were detected by Western blot and immunofluorescence respectively. THP-1 and primary bone marrow-derived monocytes (BMDMs) were also used to demonstrate effect of PGRN on expressions and secretion of inflammatory cytokines induced by LPS.

resultsIn RAW264.7 cells, rPGRN at concentrations below 80 ng/ml significantly promoted cell proliferation in dose dependent fashion. rPGRN significantly inhibited LPS-induced change of phenotype (CD86/CD206 ratio) and function (tumor necrosis factor (TNF-α) and inducible nitric oxide synthase (iNOS) expressions). LPS-stimulated secretion of TNF-α and activated phosphorylation of IKKα/β, IкBα, p65, JNK and p38 and the nucleus translocation of NF-кB p65 were also significantly downregulated by rPGRN. In addition, recombinant TNF-α (rTNF-α) significantly boosted TNF-α and iNOS expression vs the control group. Moreover, anti-TNF-α significantly inhibited LPS-induced TNF-α and iNOS expression. In THP-1 and BMDM cells, reversing effect of rPGRN on LPS-enhanced expressions of TNF-α and iNOS and secretion of TNF-α was further demonstrated.

conclusionsPGRN down-regulates LPS-induced macrophage M1 polarization in phenotype and function via NF-κB/MAPK signaling pathways.

Indexed as

AnimalsBiomarkersCell LineCell ProliferationCytokinesHumansInflammationLipopolysaccharidesMacrophage ActivationMacrophagesMAP Kinase Signaling SystemMiceMice, Inbred C57BLMitogen-Activated Protein KinasesNF-kappa BProgranulinsBiomarkersCytokinesLipopolysaccharidesMitogen-Activated Protein KinasesNF-kappa BProgranulinsTranscription Factor RelATumor Necrosis Factor-alphaLipopolysaccharide (LPS)Macrophage polarizationMAPKNF-κBPGRN

Identifiers

PMID32503416
PMCPMC7275413
OpenAlexW3033135976

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.