Evidence map›Paper›PMID 32587089›Full record

ArticleThe Journal of biological chemistry2020

Ubiquitination of interleukin-1α is associated with increased pro-inflammatory polarization of murine macrophages deficient in the E3 ligase ITCH.

Xi Lin, Hengwei Zhang, Brendan F Boyce, Lianping Xing

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Xi LinDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York, USA.ORCID 0000-0001-5905-5311
Hengwei ZhangDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York, USA.
Brendan F BoyceDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York, USA.
Lianping XingDepartment of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, New York, USA Lianping_xing@urmc.rochester.edu.
University of Rochester Medical Center · US

Funding

VITamin D and OmegA-3 TriaL (VITAL): Interrelationship of Vitamin D and Vitamin K on BoneR01AR059775 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI LEBOFF, MERYL SUSAN · 2012 to 2022
$3.9M
Synovial lymphatics and osteoarthritis in agingR01AG059775 · NIA · UNIVERSITY OF ROCHESTER · PI XING, LIANPING · 2020 to 2024
$1.9M
Protein modification in bone cell regulationR21AR069789 · NIAMS · UNIVERSITY OF ROCHESTER · PI BOECKMAN, ROBERT K, XING, LIANPING · 2016 to 2017
$372k
NIAMS NIH HHS R01 AR059775NIAMS NIH HHS R21 AR069789NIA NIH HHS R01 AG059775
6 · The paper itself

Abstract

Macrophages play critical roles in homeostasis and inflammation. Macrophage polarization to either a pro-inflammatory or anti-inflammatory status is controlled by activating inflammatory signaling pathways. Ubiquitination is a posttranslational modification that regulates these inflammatory signaling pathways. However, the influence of protein ubiquitination on macrophage polarization has not been well studied. We hypothesized that the ubiquitination status of key proteins in inflammatory pathways contributes to macrophage polarization, which is regulated by itchy E3 ubiquitin ligase (ITCH), a negative regulator of inflammation. Using ubiquitin proteomics, we found that ubiquitination profiles are different among polarized murine macrophage subsets. Interestingly, interleukin-1α (IL-1α), an important pro-inflammatory mediator, was specifically ubiquitinated in lipopolysaccharide-induced pro-inflammatory macrophages, which was enhanced in ITCH-deficient macrophages. The ITCH-deficient macrophages had increased levels of the mature form of IL-1α and exhibited pro-inflammatory polarization, and reduced deubiquitination of IL-1α protein. Finally, IL-1α neutralization attenuated pro-inflammatory polarization of the ITCH-deficient macrophages. In conclusion, ubiquitination of IL-1α is associated with increased pro-inflammatory polarization of macrophages deficient in the E3 ligase ITCH.

Indexed as

UbiquitinationAnimalsCells, CulturedFemaleGene DeletionInflammationInterleukin-1alphaMacrophagesMaleMice, Inbred C57BLUbiquitinUbiquitin-Protein LigasesInterleukin-1alphaItch protein, mouseUbiquitinUbiquitin-Protein Ligasesdeubiquitinationdeubiquitylation (deubiquitination)IL-1αinflammationinnate immunityinterleukin 1 (IL-1)Interleukin-1αItchitchy E3 ubiquitin protein ligase (ITCH)macrophagemacrophage polarizationposttranslational modificationproteomicsubiquitinationubiquitylation (ubiquitination)

Identifiers

PMID32587089
PMCPMC7450106
OpenAlexW3037911905

What OpenQuestion holds

Textmetadata
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.