Evidence map›Paper›PMID 25583990›Full record

ArticleThe Journal of biological chemistry2015

The histone methyltransferase Smyd2 is a negative regulator of macrophage activation by suppressing interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) production.

Guiliang Xu, Guilin Liu, Sidong Xiong, Haiyan Liu, Xi Chen, Biao Zheng

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Review
  9. Review
  10. Review
  11. The Role of Protein Methyltransferases in Immunity.Molecules (Basel, Switzerland) · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
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10 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

Guiliang XuFrom the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.
Guilin LiuFrom the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.
Sidong XiongFrom the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.
Haiyan LiuFrom the Jiangsu Key Laboratory of Infection and Immunity, Institute of Biological and Medical Sciences, Soochow University, Suzhou 215123, China.
Xi Chenthe Shanghai Key Laboratory of Regulatory Biology, School of Biological Sciences, East China Normal University, Shanghai 200241, China, and the Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas 77030 xichen0919@gmail.com.
Biao Zhengthe Shanghai Key Laboratory of Regulatory Biology, School of Biological Sciences, East China Normal University, Shanghai 200241, China, and the Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas 77030 bzheng@bcm.edu.
Soochow University · CNBaylor College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SET and MYND domain-containing 2 (Smyd2), a histone 3 lysine 4- and histone 3 lysine 36 (H3K36)-specific methyltransferase, plays critical roles in cardiac development and tumorigenesis. However, the role of Smyd2 in immunity and inflammation remains poorly understood. In this study, we report that Smyd2 is a novel negative regulator for macrophage activation and M1 polarization. Elevated Smyd2 expression suppresses the production of proinflammatory cytokines, including IL-6 and TNF, and inhibits the expression of important cell surface molecules, including major MHC-II and costimulatory molecules. Furthermore, macrophages with high Smyd2 expression inhibit Th-17 cell differentiation but promote regulatory T cell differentiation as a result of increased TGF-β production and decreased IL-6 secretion. In macrophages, Smyd2 specifically facilitates H3K36 dimethylation at Tnf and Il6 promoters to suppress their transcription and inhibits NF-κB and ERK signaling. Therefore, our data demonstrate that epigenetic modification by Smyd2-mediated H3K36 dimethylation at Tnf and Il6 promoters plays an important role in the regulation of macrophage activation during inflammation.

Indexed as

Gene Expression RegulationAnimalsBlotting, WesternCell DifferentiationCell LineCells, CulturedFlow CytometryHistone-Lysine N-MethyltransferaseHistonesInterleukin-6LysineMacrophage ActivationMacrophagesMAP Kinase Signaling SystemMethylationMice, Inbred C57BLHistone-Lysine N-MethyltransferaseHistonesInterleukin-6LysineNF-kappa BSmyd2 protein, mouseTumor Necrosis Factor-alphaAutoimmunityChiPImmunologyMacrophageSignaling

Identifiers

PMID25583990
PMCPMC4342458
OpenAlexW2065215000

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.