Evidence map›Paper›PMID 35439173›Full record

ArticleThe Journal of clinical investigation2022

Soluble CD13 induces inflammatory arthritis by activating the bradykinin receptor B1.

Pei-Suen Tsou, Chenyang Lu, Mikel Gurrea-Rubio, Sei Muraoka, Phillip L Campbell, Qi Wu, Ellen N Model, Matthew E Lind, Sirapa Vichaikul, Megan N Mattichak and 21 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

31 authors at 3 institutions in 2 countries.

Pei-Suen TsouDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Chenyang LuDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Mikel Gurrea-RubioDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Sei MuraokaDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Phillip L CampbellDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Qi WuDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Ellen N ModelDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Matthew E LindDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Sirapa VichaikulDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Megan N MattichakDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
William D BrodieDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Jonatan L HervosoDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Sarah OryDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Camila I AmaristaDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Rida PervezDepartment of Orthopedic Surgery, University of Michigan Health System, Ann Arbor, Michigan, USA.
Lucas JungingerDepartment of Orthopedic Surgery, University of Michigan Health System, Ann Arbor, Michigan, USA.
Mustafa AliDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Gal HodishDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Morgan M O'MaraDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Jeffrey H RuthDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Aaron M RobidaPharmacology Department.
Andrew J AltPharmacology Department.
Chengxin ZhangDepartment of Computational Medicine and Bioinformatics.
Andrew G UrquhartDepartment of Orthopedic Surgery, University of Michigan Health System, Ann Arbor, Michigan, USA.
Jeffrey N LawtonDepartment of Orthopedic Surgery, University of Michigan Health System, Ann Arbor, Michigan, USA.
Kevin C ChungDepartment of Orthopedic Surgery, University of Michigan Health System, Ann Arbor, Michigan, USA.
Tristan MaerzDepartment of Orthopedic Surgery, University of Michigan Health System, Ann Arbor, Michigan, USA.
Thomas L SaundersDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Vincent E GroppiCenter for Discovery of New Medicine, University of Michigan, Ann Arbor, Michigan, USA.
David A FoxDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
M Asif AminDivision of Rheumatology and Clinical Autoimmunity Center of Excellence, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
University of Michigan · USMichigan Medicine · USSichuan University · CN

Funding

Autoimmunity Center of Excellence Clinical Research ProgramUM1AI110498 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WOFSY, DAVID · 2014 to 2019
$31.4M
Structure, Composition, & Histology Core - Core BP30AR069620 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KARL J JEPSEN · 2016 to 2026
$8.4M
University of Michigan Skin Biology and Diseases Resource-based CenterP30AR075043 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Johann Eli Gudjonsson · 2019 to 2026
$6.6M
TRAINING OF ARTHRITIS RESEARCH SCIENTISTST32AR007080 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Jason Knight · 1986 to 2026
$6.3M
University of Michigan Clinical Autoimmunity Center of ExcellenceUM1AI144298 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN, KHANNA, DINESH · 2019 to 2023
$546k
Roles of soluble CD13 and its receptor in angiogenesis, monocyte recruitment, and joint inflammationR56AR076384 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 2020 to 2020
$447k
Proinflammatory and Autoantigenic Properties of a Novel Citrullinated Form of IL-6 in Rheumatoid ArthritisR21AR072931 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 2018 to 2019
$377k
NIAID NIH HHS UM1 AI110498NIAID NIH HHS UM1 AI144298NIAMS NIH HHS P30 AR069620NIAMS NIH HHS P30 AR075043NIAMS NIH HHS R21 AR072931NIAMS NIH HHS R56 AR076384NIAMS NIH HHS T32 AR007080
6 · The paper itself

Abstract

CD13, an ectoenzyme on myeloid and stromal cells, also circulates as a shed, soluble protein (sCD13) with powerful chemoattractant, angiogenic, and arthritogenic properties, which require engagement of a G protein-coupled receptor (GPCR). Here we identify the GPCR that mediates sCD13 arthritogenic actions as the bradykinin receptor B1 (B1R). Immunofluorescence and immunoblotting verified high expression of B1R in rheumatoid arthritis (RA) synovial tissue and fibroblast-like synoviocytes (FLSs), and demonstrated binding of sCD13 to B1R. Chemotaxis, and phosphorylation of Erk1/2, induced by sCD13, were inhibited by B1R antagonists. In ex vivo RA synovial tissue organ cultures, a B1R antagonist reduced secretion of inflammatory cytokines. Several mouse arthritis models, including serum transfer, antigen-induced, and local innate immune stimulation arthritis models, were attenuated in Cd13-/- and B1R-/- mice and were alleviated by B1R antagonism. These results establish a CD13/B1R axis in the pathogenesis of inflammatory arthritis and identify B1R as a compelling therapeutic target in RA and potentially other inflammatory diseases.

Indexed as

Arthritis, RheumatoidSynoviocytesAnimalsBradykininCD13 AntigensDisease Models, AnimalFibroblastsMiceReceptor, Bradykinin B1Receptors, G-Protein-CoupledSynovial MembraneBradykininCD13 AntigensReceptor, Bradykinin B1Receptors, G-Protein-CoupledArthritisAutoimmunityChemokinesG protein–coupled receptors

Identifiers

PMID35439173
PMCPMC9151693
OpenAlexW4224269270

What OpenQuestion holds

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Read underepoch 390

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.