Evidence map›Paper›PMID 32022446›Full record

ArticleJournal of cellular and molecular medicine2020

Foxf2 and Smad6 co-regulation of collagen 5A2 transcription is involved in the pathogenesis of intrauterine adhesion.

Guobin Chen, Limin Liu, Jing Sun, Liying Zeng, Huihua Cai, Yuanli He

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.4field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 38 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

6 authors at 3 institutions in 1 country.

Guobin ChenDepartment of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0003-3145-7321
Limin LiuDepartment of Obstetrics and Gynecology, Shenzhen Maternity and Childcare Hospital, Shenzhen, China.
Jing SunDepartment of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Liying ZengDepartment of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Huihua CaiDepartment of Obstetrics and Gynecology, Guangdong Provincial People`s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Yuanli HeDepartment of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Zhujiang Hospital · CNGuangdong Academy of Medical Sciences · CNShenzhen Maternity and Child Healthcare Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The replacement of normal endometrial epithelium by fibrotic tissue is the pathological feature of intrauterine adhesion (IUA), which is caused by trauma to the basal layer of the endometrium. COL5A2 is a molecular subtype of collagen V that regulates collagen production in fibrotic tissue. Here, we investigated the roles of Foxf2 and Smad6 in regulating the transcription of COL5A2 and their involvement in the pathogenesis of IUA. Small interference-mediated Foxf2 (si-Foxf2) silencing and pcDNA3.1-mediated Smad6 (pcDNA3.1-Smad6) up-regulation were performed in a TGF-β1-induced human endometrial stromal cell line (HESC) fibrosis model. Assessment of collagen expression by Western blotting, immunofluorescence and qRT-PCR showed that COL5A2, COL1A1 and FN were significantly down-regulated in response to si-Foxf2 and pcDNA3.1-Smad6. Transfection of lentivirus vector-Foxf2 (LV-Foxf2) and pcDNA3.1-Smad6 into HESCs and qRT-PCR showed that Foxf2 promoted COL5A2 expression and Smad6 inhibited Foxf2-induced COL5A2 expression. Co-immunoprecipitation, chromatin immunoprecipitation and dual-luciferase reporter assays to detect the interaction between Foxf2 and Smad6 and their role in COL5A2 transcription showed that Foxf2 interacted with Smad6 and bond the same promoter region of COL5A2. In a rat IUA model, injection of ADV2-Foxf2-1810 and ADV4-Smad6 into the uterine wall showed that Foxf2 down-regulation and Smad6 up-regulation decreased fibrosis and the expression of COL5A2 and COL1A1, as detected by haematoxylin/eosin, Masson trichrome staining and immunohistochemistry. Taken together, these results suggested that Foxf2 interacted with Smad6 and co-regulated COL5A2 transcription in the pathogenesis of IUA, whereas they played opposite roles in fibrosis.

Indexed as

AnimalsCell CycleCell LineCell ProliferationCollagen Type VDisease Models, AnimalDown-RegulationEndometriumFemaleFibrosisForkhead Transcription FactorsHumansRats, Sprague-DawleySmad6 ProteinStromal CellsTissue AdhesionsCollagen Type VForkhead Transcription FactorsFOXF2 protein, humanSmad6 ProteinTransforming Growth Factor beta1fibrosisFoxf2intrauterine adhesionSmad6

Identifiers

PMID32022446
PMCPMC7077542
OpenAlexW3004959281

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.