Evidence map›Paper›PMID 30229869›Full record

ArticleClinical and experimental immunology2019

Blocking of YY1 reduce neutrophil infiltration by inhibiting IL-8 production via the PI3K-Akt-mTOR signaling pathway in rheumatoid arthritis.

J Lin, Y He, B Wang, Z Xun, S Chen, Z Zeng, Q Ou

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 53 citations in OpenAlex.

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  15. eLife · 2022
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  18. Effect of moxibustion on autophagy and the inflammatory response of synovial cells in rheumatoid arthritis model rat.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022
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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

7 authors at 2 institutions in 1 country.

J LinDepartment of Laboratory Medicine, the First Affiliated Hospital of Fujian Medical University, Fujian, China.
Y HeDepartment of Laboratory Medicine, the First Affiliated Hospital of Fujian Medical University, Fujian, China.
B WangDepartment of Laboratory Medicine, the First Affiliated Hospital of Fujian Medical University, Fujian, China.
Z XunDepartment of Laboratory Medicine, the First Affiliated Hospital of Fujian Medical University, Fujian, China.
S ChenDepartment of Laboratory Medicine, the First Affiliated Hospital of Fujian Medical University, Fujian, China.
Z ZengDepartment of Hematology and Rheumatology, the First Affiliated Hospital of Fujian Medical University, Fujian, China.
Q OuDepartment of Laboratory Medicine, the First Affiliated Hospital of Fujian Medical University, Fujian, China.
First Affiliated Hospital of Fujian Medical University · CNFujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous study revealed that Yin Yang 1(YY1) played an important part in promoting interleukin (IL)-6 production in rheumatoid arthritis (RA). However, whether YY1 has any role in regulation of IL-8 in RA remains unclear. YY1 and IL-8 expression in RA patients were analyzed by real-time polymerase chain reaction (PCR). Ingenuity pathway analysis (IPA) was used to analyze the signaling pathway involved in YY1-induced IL-8 production. The expression of YY1 and proteins involved in the pathway were detected by Western blot and enzyme-linked immunosorbent assay (ELISA). Migration of neutrophils was performed by chemotaxis assay. In this study, we found that high expression of IL-8 was positively associated with YY1 expression in RA. Blocking YY1 expression by YY1-short hairpin (sh)RNA lentivirus reduced IL-8 production. Mechanistically, we showed YY1 activated IL-8 production via the phosphatidylinositol-3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway. Further, using a co-culture system consisting of peripheral blood mononuclear cells (PBMC) and neutrophils, we found that migration of neutrophils would be inhibited by YY1 RNA interference. Finally, using the collagen-induced arthritis animal model, we showed that treatment with the YY1-shRNA lentivirus led to reduction of IL-8 levels and attenuation of inflammation and neutrophil infiltration in vivo. Our results reveal a role of YY1 involved in neutrophil infiltration in RA via the PI3K/Akt/mTOR/IL-8 signaling pathway. YY1 may be a new therapeutic target for treatment of RA.

Indexed as

Arthritis, RheumatoidChemotaxisHumansInterleukin-8MAP Kinase Signaling SystemNeutrophil InfiltrationNeutrophilsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA InterferenceRNA, Small InterferingTOR Serine-Threonine KinasesYY1 Transcription FactorCXCL8 protein, humanInterleukin-8MTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine KinasesYY1 protein, humanYY1 Transcription Factorinterleukin-8neutrophilsrheumatoid arthritisYY1

Identifiers

PMID30229869
PMCPMC6330653
OpenAlexW2892370542

What OpenQuestion holds

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Registered trials

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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.