Evidence map›Paper›PMID 32638833›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2020

Estrogen attenuates TGF-β1-induced EMT in intrauterine adhesion by activating Wnt/β-catenin signaling pathway.

Jia Cao, Dan Liu, Shiyun Zhao, Liwei Yuan, Yani Huang, Jingwen Ma, Zhijuan Yang, Bin Shi, Libin Wang, Jun Wei

Open access · goldAbstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 43 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

10 authors at 1 institution in 1 country.

Jia CaoCollege of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, China.
Dan LiuCollege of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, China.
Shiyun ZhaoCollege of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, China.
Liwei YuanCollege of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, China.
Yani HuangCollege of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, China.
Jingwen MaDepartment of Gynecology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Zhijuan YangDepartment of Gynecology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Bin ShiDepartment of Beijing National Biochip Research Center Sub-Center in Ningxia, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, China.
Libin WangCollege of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, China.
Jun WeiCollege of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, China.
Ningxia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although estrogen has crucial functions for endometrium growth, the specific dose and underlying molecular mechanism in intrauterine adhesion (IUA) remain unclear. In this study, we aimed to investigate the effects of estrogen on epithelial-mesenchymal transition (EMT) in normal and fibrotic endometrium, and the role of estrogen and Wnt/β-catenin signaling in the formation of endometrial fibrosis. CCK-8 and immunofluorescence assay were performed to access the proliferation of different concentrations of estrogen on normal human endometrial epithelial cells (hEECs). qRT-PCR and western blot assay were utilized to explore the effect of estrogen on EMT in normal and fibrotic endometrium, and main components of Wnt/β-catenin signaling pathway in vitro. Hematoxylin and eosin and Masson staining were used to evaluate the effect of estrogen on endometrial morphology and fibrosis in vivo. Our results indicated that the proliferation of normal hEECs was inhibited by estrogen at a concentration of 30 nM accompanied by upregulation of mesenchymal markers and downregulation of epithelial markers. Interestingly, in the model of transforming growth factor β1 (TGF-β1)-induced endometrial fibrosis, the same concentration of estrogen inhibited the process of EMT, which might be partially mediated by regulation of the Wnt/β-catenin pathway. In addition, relatively high doses of estrogen efficiently increased the number of endometrial glands and reduced the area of fibrosis as determined by the reduction of EMT in IUA animal models. Taken together, our results demonstrated that an appropriate concentration of estrogen may prevent the occurrence and development of IUA by inhibiting the TGF-β1-induced EMT and activating the Wnt/β-catenin pathway.

Indexed as

Epithelial-Mesenchymal TransitionTransforming Growth Factor beta1Uterine DiseasesAnimalsEstrogensFemaleHumansWnt Signaling PathwayEstrogensTransforming Growth Factor beta1

Identifiers

PMID32638833
PMCPMC7346761
OpenAlexW3041699810

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.