Evidence map›Paper›PMID 28661480›Full record

ArticleCell death & disease2017

Role of peroxiredoxin2 downregulation in recurrent miscarriage through regulation of trophoblast proliferation and apoptosis.

Fan Wu, Fuju Tian, Weihong Zeng, Xiaorui Liu, Jianxia Fan, Yi Lin, Yan Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.9field-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

43 citing papers in PubMed, 90 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

7 authors at 3 institutions in 1 country.

Fan WuInstitute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine, the International Peace Maternity &Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fuju TianInstitute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine, the International Peace Maternity &Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Weihong ZengInstitute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine, the International Peace Maternity &Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaorui LiuInstitute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine, the International Peace Maternity &Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jianxia FanInstitute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine, the International Peace Maternity &Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yi LinInstitute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine, the International Peace Maternity &Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yan ZhangDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Shanghai Jiao Tong University · CNInternational Peace Maternity & Child Health Hospital · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peroxiredoxin (Prdx) 2 is an antioxidant protein that utilizes its redox-sensitive cysteine groups to reduce hydrogen peroxide molecules and protect cells against oxidative damage from reactive oxygen species (ROS). However, its function in trophoblasts at the maternal-fetal interface has not been clarified yet. In this study, significantly lower Prdx2 expression was found in the first-trimester villous cytotrophoblasts of patients with recurrent miscarriage (RM) than in cytotrophoblasts from healthy controls. Further, Prdx2 knockdown inhibited proliferation and increased apoptosis of trophoblast cells. The reason for this may be an increase in the level of cellular ROS after knockdown of Prdx2, which may subsequently lead to an increase in the expression of phosphorylated p53 (p-p53) and p38-MAPK/p21. Prdx2 knockdown also impaired the fusion of BeWo cells induced by forskolin. Bioinformatics analysis identified a c-Myc-binding site in the Prdx2 promoter region, and chromatin immunoprecipitation verified that c-Myc directly bound to a site in this locus. Suppression and overexpression of c-Myc resulted in reduction and increase of Prdx2 expression respectively. Furthermore, we demonstrated that c-Myc was downregulated in the first-trimester cytotrophoblasts of patients with RM, and its downregulation is also related with inhibited cell proliferation, increased apoptosis, as well as upregulated p21 expression and p-p53/p53 ratio. Our findings indicate that Prdx2 might have an important role in the regulation of trophoblast proliferation and apoptosis during early pregnancy, and that its expression is mediated by c-Myc. Thus, these two proteins may be involved in the pathogenesis of RM and may represent potential therapeutic targets.

Indexed as

Abortion, HabitualAntioxidantsApoptosisCell ProliferationChorionic VilliFemaleGene Expression Regulation, DevelopmentalGene Knockdown TechniquesHumansHydrogen PeroxideOxidative StressPeroxiredoxinsPregnancyPrimary Cell CulturePromoter Regions, GeneticProto-Oncogene Proteins c-mycAntioxidantsHydrogen PeroxideMYC protein, humanPeroxiredoxinsProto-Oncogene Proteins c-mycReactive Oxygen Species

Identifiers

PMID28661480
PMCPMC5520946
OpenAlexW2731179570

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.