Evidence map›Paper›PMID 36359746›Full record

ArticleCells2022

A Study on MDA5 Signaling in Splenic B Cells from an Imiquimod-Induced Lupus Mouse Model with Proteomics.

Yu-Jih Su, Fu-An Li, Jim Jinn-Chyuan Sheu, Sung-Chou Li, Shao-Wen Weng, Feng-Chih Shen, Yen-Hsiang Chang, Huan-Yuan Chen, Chia-Wei Liou, Tsu-Kung Lin and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. 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

12 authors at 3 institutions in 1 country.

Yu-Jih SuDepartment of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.ORCID 0000-0002-7274-3458
Fu-An LiInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.ORCID 0000-0002-0580-7765
Jim Jinn-Chyuan SheuInstitute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung 804201, Taiwan.
Sung-Chou LiCenter for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.ORCID 0000-0002-3016-9718
Shao-Wen WengDepartment of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.
Feng-Chih ShenDepartment of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.ORCID 0000-0002-9936-6074
Yen-Hsiang ChangCenter for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.ORCID 0000-0003-4491-0076
Huan-Yuan ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.ORCID 0000-0002-6390-1178
Chia-Wei LiouCenter for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.ORCID 0000-0002-9003-4065
Tsu-Kung LinCenter for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.
Jiin-Haur ChuangCenter for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.
Pei-Wen WangDepartment of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan.ORCID 0000-0002-6369-8712
Chang Gung University · TWInstitute of Biomedical Sciences, Academia Sinica · TWNational Sun Yat-sen University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSeveral environmental stimuli may influence lupus, particularly viral infections. In this study, we used an imiquimod-induced lupus mouse model focused on the TLR7 pathway and proteomics analysis to determine the specific pathway related to viral infection and the related protein expressions in splenic B cells to obtain insight into B-cell responses to viral infection in the lupus model. MATERIALS AND

methodsWe treated FVB/N wild-type mice with imiquimod for 8 weeks to induce lupus symptoms and signs, retrieved splenocytes, selected B cells, and conducted the proteomic analysis. The B cells were co-cultured with CD40L+ feeder cells for another week before performing Western blot analysis. Panther pathway analysis was used to disclose the pathways activated and the protein-protein interactome was analyzed by the STRING database in this lupus murine model.

resultsThe lupus model was well established and well demonstrated with serology evidence and pathology proof of lupus-mimicking organ damage. Proteomics data of splenic B cells revealed that the most important activated pathways (fold enrichment > 100) demonstrated positive regulation of the MDA5 signaling pathway, negative regulation of IP-10 production, negative regulation of chemokine (C-X-C motif) ligand 2 production, and positive regulation of the RIG-I signaling pathway. A unique protein-protein interactome containing 10 genes was discovered, within which ISG15, IFIH1, IFIT1, DDX60, and DHX58 were demonstrated to be downstream effectors of MDA5 signaling. Finally, we found B-cell intracellular cytosolic proteins via Western blot experiment and continued to observe MDA5-related pathway activation.

conclusionIn this experiment, we confirmed that the B cells in the lupus murine model focusing on the TLR7 pathway were activated through the MDA5 signaling pathway, an important RNA sensor implicated in the detection of viral infections and autoimmunity. The MDA5 agonist/antagonist RNAs and the detailed molecular interactions within B cells are worthy of further investigation for lupus therapy.

Indexed as

Interferon-Induced Helicase, IFIH1Virus DiseasesAnimalsDEAD-box RNA HelicasesDisease Models, AnimalImiquimodLupus Erythematosus, SystemicMiceProteomicsSignal TransductionToll-Like Receptor 7DEAD-box RNA HelicasesIfih1 protein, mouseImiquimodInterferon-Induced Helicase, IFIH1Toll-Like Receptor 7B celllupusMDA5proteomicssplenocyte

Identifiers

PMID36359746
PMCPMC9657434
OpenAlexW4307271209

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.