Evidence map›Paper›PMID 26648169›Full record

ArticleScientific reports2015

A20 regulates IL-1-induced tolerant production of CXC chemokines in human mesangial cells via inhibition of MAPK signaling.

Hongbo Luo, Yuming Liu, Qian Li, Lingjuan Liao, Ruili Sun, Xueting Liu, Manli Jiang, Jinyue Hu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. A20 as a Potential Therapeutic Target for COVID-19.Immunity, inflammation and disease · 2025
    Review
  2. A20 in Kidney Transplantation and Autoimmunity.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. IL-1α and IL-1β promote NOD2-induced immune responses by enhancing MAPK signaling.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. 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

8 authors at 2 institutions in 1 country.

Hongbo LuoMedical Research Center, Changsha Central Hospital, Changsha, 410004, China.
Yuming LiuDepartment of Urology, Changsha Central Hospital, Changsha, 410004, China.
Qian LiDepartment of Nephrology, Changsha Central Hospital, Changsha, 410004, China.
Lingjuan LiaoMedical Research Center, Changsha Central Hospital, Changsha, 410004, China.
Ruili SunDepartment of Laboratory Medicine, XinXiang Medical University, XinXiang, 453003, China.
Xueting LiuMedical Research Center, Changsha Central Hospital, Changsha, 410004, China.
Manli JiangMedical Research Center, Changsha Central Hospital, Changsha, 410004, China.
Jinyue HuMedical Research Center, Changsha Central Hospital, Changsha, 410004, China.
Changsha Central Hospital · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokines and chemokine receptors are involved in the resolution or progression of renal diseases. Locally secreted chemokines mediated leukocyte recruitment during the initiation and amplification phase of renal inflammation. However, the regulation of chemokine induction is not fully understood. In this study, we found that IL-1 induced a significant up-regulation of CXC chemokines CXCL1, 2, and 8 at both mRNA and protein levels in human mesangial cells. The induction of chemokines was tolerant, as the pre-treatment of HMC with IL-1 down-regulated the induction of chemokines induced by IL-1 re-stimulation. IL-1 up-regulated the ubiquintin-editing enzyme A20. A20 over-expression down-regulated IL-1-induced up-regulation of chemokines, and A20 down-regulation reversed chemokine inhibition induced by IL-1 pre-treatment, suggested that A20 played important roles in the tolerant production of chemokines. Unexpectedly, A20 over- expression inhibited the activation of ERK, JNK, and P38, but did not inhibit the activation of NF-κB. In addition, both IL-1 treatment and A20 over-expression induced the degradation of IRAK1, an important adaptor for IL-1R1 signaling, and A20 inhibition by RNA interference partly reversed the degradation of IRAK1. Taken together, IL-1-induced A20 negatively regulated chemokine production, suggesting that A20 may be an important target for the prevention and control of kidney inflammation.

Indexed as

MAP Kinase Signaling SystemChemokines, CXCDNA-Binding ProteinsGene Expression RegulationHumansInterleukin-1Interleukin-1 Receptor-Associated KinasesIntracellular Signaling Peptides and ProteinsMesangial CellsNF-kappa BNuclear ProteinsProteolysisReceptors, Interleukin-1 Type IReceptors, Interleukin-1 Type IITumor Necrosis Factor alpha-Induced Protein 3Chemokines, CXCDNA-Binding ProteinsInterleukin-1Interleukin-1 Receptor-Associated KinasesIntracellular Signaling Peptides and ProteinsIRAK1 protein, humanNF-kappa BNuclear ProteinsReceptors, Interleukin-1 Type IReceptors, Interleukin-1 Type IITNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID26648169
PMCPMC4673611
OpenAlexW2195190261

What OpenQuestion holds

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LicenceCC BY
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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.