Evidence map›Paper›PMID 35100093›Full record

ArticleBioengineered2022

Upstream stimulatory factor 2 (USF2) induced upregulation of triggering receptor expressed on myeloid cells 1 (TREM1) promotes endometritis by regulating toll-like receptor (TLR) 2/4-nuclear factor-kappaB (NF-κB) signaling pathway.

Miao Zhang, Chengkun Yin, Yan Chen, Juan Wang, Jing Jiang

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  3. Stored RBC transfusions leads to the systemic inflammatory response syndrome in anemic murine neonates.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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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

5 authors at 2 institutions in 1 country.

Miao ZhangDepartment of Gynecology and Obstetrics, The Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Chengkun YinDepartment of Radiology, Suining Central Hospital, Suining, China.
Yan ChenDepartment of Gynecology and Obstetrics, The Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Juan WangDepartment of Gynecology and Obstetrics, The Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Jing JiangDepartment of Gynecology and Obstetrics, The Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Affiliated Hospital of North Sichuan Medical College · CNSuizhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triggering receptor expressed on myeloid cells 1 (TREM1) participates in the development of endometritis. This study aims at identifying the effects and interaction of TREM1 and upstream stimulatory factor 2 (USF2) in endometritis by using a model of lipopolysaccharide (LPS)-induced human endometrial epithelial cells (HEnEpCs). ELISA was performed to determine the levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF-α) after LPS stimulation. TREM1 and USF2 expression was examined with RT-qPCR and Western blot. The JASPAR database was employed to predict the binding site between USF2 and TREM1, which was confirmed by luciferase reporter and chromatin immunoprecipitation assays. After TREM1 overexpression, IL-6, IL-1β, and TNF-α expression was detected by ELISA. Next, the binding of TREM1 to toll-like receptor (TLR) 2/4 was examined with co-immunoprecipitation. Then, proteins in TLR2/4-nuclear factor-kappaB (NF-κB) signaling in HEnEpCs under LPS condition were assessed by Western blot or immunofluorescence before and after TREM1 knockdown. Finally, TLR2 or TLR4 was silenced to explore whether intervene TLR2/4-NF-κB signaling pathway could rescue TREM1-overexpression-induced inflammation in LPS-induced HEnEpCs. Results revealed that upregulated TREM1 was observed in LPS-challenged HEnEpCs. Next, USF2 was found to have transcriptionally active TREM1 expression. Additionally, USF2 knockdown decreased the levels of IL-6, IL-1β, and TNF-α, whereas this effect was rescued after TREM1 overexpression. Besides, TREM1 could bind to TLR2/4 to regulate NF-κB signaling. Moreover, the intervention of TLR2/4-NF-κB signaling pathway rescued TREM1-overexpression-induced inflammation in LPS-stimulated HEnEpCs. Collectively, USF2 promotes endometritis by upregulating TREM1, thereby activating TLR2/4-NF-κB pathway.

Indexed as

Signal TransductionUp-RegulationEndometritisEndometriumEpithelial CellsFemaleHumansNF-kappa BToll-Like Receptor 2Toll-Like Receptor 4Triggering Receptor Expressed on Myeloid Cells-1Upstream Stimulatory FactorsNF-kappa BTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4TREM1 protein, humanTriggering Receptor Expressed on Myeloid Cells-1Upstream Stimulatory FactorsUSF2 protein, humanEndometritisNF-κBTLR2/4TREM1USF2

Identifiers

PMID35100093
PMCPMC8973694
OpenAlexW4210766290

What Socratic 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 Socratic graph.