Evidence map›Paper›PMID 30793522›Full record

ArticleJournal of cellular and molecular medicine2019

β-arrestin 2 negatively regulates NOD2 signalling pathway through association with TRAF6 in microglia after cerebral ischaemia/reperfusion injury.

Lin Chen, Lingjun Kong, Xinbing Wei, Yimeng Wang, Bing Wang, Xiumei Zhang, Jinpeng Sun, Huiqing Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Pathogenic Functions of Tumor Necrosis Factor Receptor-Frontiers in molecular neuroscience · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. G Protein-Coupled Receptor Systems and Their Role in Cellular Senescence.Computational and structural biotechnology journal · 2019
    Review
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.

Lin ChenDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, P.R. China.
Lingjun KongDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, P.R. China.
Xinbing WeiDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, P.R. China.
Yimeng WangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, P.R. China.
Bing WangDepartment of Emergency, The people's Hospital of Huaiyin, Jinan, Shandong, P.R. China.
Xiumei ZhangDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, P.R. China.
Jinpeng SunKey Laboratory Experimental Teratology of the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Medicine, Shandong University, Jinan, P.R. China.
Huiqing LiuDepartment of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, P.R. China.ORCID 0000-0001-8866-3957
Shandong University · CNFourth People’s Hospital of Jinan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that nucleotide-binding oligomerization domain-containing protein (NOD) 2 was involved in the inflammatory responses to cerebral ischaemia/reperfusion (I/R) insult. However, the mechanism by which NOD2 participates in brain ischaemic injury and the regulation of NOD2 in the process are still obscure. Increased β-arrestin 2 (ARRB2) expression was observed in microglia following cerebral I/R in wild-type mice besides the up-regulation of NOD2 and TRAF6. Stimulation of NOD2 by muramyl dipeptide (MDP) in BV2 cells induced the activation of NF-κB by the phosphorylation of p65 subunit and the degradation of IκBα. Meanwhile, the protein level of Cyclooxygenase-2 (COX-2), the protein expression and activity of MMP-9 were significantly increased in BV2 cells after administration of MDP. Furthermore, overexpression of ARRB2 significantly suppressed the inflammation induced by MDP, silence of ARRB2 significantly enhanced the inflammation induced by MDP in BV2 cells. In addition, we observed endogenous interaction of TRAF6 and ARRB2 after stimulation of MDP or cerebral I/R insult, indicating ARRB2 negatively regulates NOD2-triggered inflammatory signalling pathway by associating with TRAF6 in microglia after cerebral I/R injury. Finally, the in vivo study clearly confirmed that ARRB2 negatively regulated NOD2-induced inflammatory response, as ARRB2 deficiency exacerbated stroke outcomes and aggravated the NF-κB signalling pathway induced by NOD2 stimulation after cerebral I/R injury. These findings revealed ARRB2 negatively regulated NOD2 signalling pathway through the association with TRAF6 in cerebral I/R injury.

Indexed as

Acetylmuramyl-Alanyl-IsoglutamineAnimalsbeta-Arrestin 2Brain IschemiaCyclooxygenase 2InflammationMatrix Metalloproteinase 9Mice, Inbred C57BLMice, KnockoutMicrogliaNF-kappa BNod2 Signaling Adaptor ProteinReperfusion InjurySignal TransductionStrokeTNF Receptor-Associated Factor 6Acetylmuramyl-Alanyl-Isoglutaminebeta-Arrestin 2Cyclooxygenase 2Matrix Metalloproteinase 9NF-kappa BNod2 Signaling Adaptor ProteinTNF Receptor-Associated Factor 6cerebral ischaemia/reperfusioninflammationNOD2β-arrestin 2

Identifiers

PMID30793522
PMCPMC6484299
OpenAlexW2915851742

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.