Evidence map›Paper›PMID 31791585›Full record

ArticleBiochemical and biophysical research communications2020

Protein phosphatase magnesium-dependent 1A induces inflammation in rheumatoid arthritis.

Beomgu Lee, You Seon Song, Christopher Rhodes, Tae Sik Goh, Jong Seong Roh, Hoim Jeong, Jisu Park, Han-Na Lee, Seung-Geun Lee, Soohyun Kim and 4 more

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. A comprehensive overview of PPM1A: From structure to disease.Experimental biology and medicine (Maywood, N.J.) · 2022
    Review
  8. Article
  9. Article
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

14 authors at 5 institutions in 2 countries.

Beomgu LeeDepartment of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea.
You Seon SongBiomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Radiology, Pusan National University Hospital, Busan, Republic of Korea.
Christopher RhodesDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, 94305, USA; VA Palo Alto Health Care System, Palo Alto, CA, 94304, USA.
Tae Sik GohBiomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Department of Orthopaedic Surgery, Pusan National University Hospital, Busan, Republic of Korea.
Jong Seong RohDepartment of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea.
Hoim JeongDepartment of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea.
Jisu ParkDepartment of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea.
Han-Na LeeBiomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Division of Rheumatology, Department of Internal Medicine, Pusan National University School of Medicine, Pusan National University Hospital, Busan, Republic of Korea.
Seung-Geun LeeBiomedical Research Institute, Pusan National University Hospital, Busan, Republic of Korea; Division of Rheumatology, Department of Internal Medicine, Pusan National University School of Medicine, Pusan National University Hospital, Busan, Republic of Korea.
Soohyun KimCollege of Veterinary Medicine, Konkuk University, Seoul, Republic of Korea.
Mingyo KimDivision of Rheumatology, Department of Internal Medicine, Gyeongsang National University School of Medicine and Hospital, Jinju, Republic of Korea.
Sang-Il LeeDivision of Rheumatology, Department of Internal Medicine, Gyeongsang National University School of Medicine and Hospital, Jinju, Republic of Korea.
Dong Hyun SohnDepartment of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, Republic of Korea. Electronic address: dhsohn@pusan.ac.kr.
William H RobinsonDivision of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, 94305, USA; VA Palo Alto Health Care System, Palo Alto, CA, 94304, USA. Electronic address: w.robinson@stanford.edu.
Pusan National University · KRGyeongsang National University Hospital · KRPusan National University Hospital · KRVA Palo Alto Health Care System · USKonkuk University · KR

Funding

Prevention Center U01: Early Targets for Antigen-Specific Tolerance Induction in Preclinical Rheumatoid ArthritisU01AI101981 · NIAID · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2012 to 2021
$6.2M
Large-Scale Characterization of Autoantibody Responses in Rheumatoid ArthritisR01AR063676 · NIAMS · STANFORD UNIVERSITY · PI ROBINSON, WILLIAM H · 2013 to 2017
$1.7M
NIAID NIH HHS U01 AI101981NIAMS NIH HHS R01 AR063676
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a highly inflammatory autoimmune disease. Although proinflammatory cytokines, including tumor necrosis factor (TNF) and interleukin (IL)-6, play a key role in the pathogenesis of RA, the causes of chronic inflammation are not fully understood. Here, we report that protein phosphatase magnesium-dependent 1A (PPM1A) levels were increased in RA synovial fluid compared with osteoarthritis (OA) synovial fluid and positively correlated with TNF levels. In addition, PPM1A expression was increased in synovial tissue from RA patients and joint tissue from a mouse model of arthritis. Finally, extracellular PPM1A induced inflammation by stimulating macrophages to produce TNF through toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein 88 (MyD88) signaling pathway. Our findings suggest that extracellular PPM1A may contribute to the pathogenesis of RA by functioning as a damage-associated molecular pattern (DAMP) to induce inflammation.

Indexed as

AgedAnimalsArthritis, RheumatoidCells, CulturedFemaleHumansInflammationMaleMiceMice, Inbred C57BLProtein Phosphatase 2CRAW 264.7 CellsSynovial FluidTumor Necrosis Factor-alphaPPM1A protein, humanPpm1a protein, mouseProtein Phosphatase 2CTumor Necrosis Factor-alphaDAMPInflammationPPM1ARheumatoid arthritis

Identifiers

PMID31791585
PMCPMC7218691
OpenAlexW2989683811

What OpenQuestion holds

Textmetadata
LicenceTDM
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.