Evidence map›Paper›PMID 32041571›Full record

ArticleBMC pregnancy and childbirth2020

Involvement of CXCL12/CXCR4 in the motility of human first-trimester endometrial epithelial cells through an autocrine mechanism by activating PI3K/AKT signaling.

Jiayi Zheng, Danni Qu, Chen Wang, Ling Ding, Wenhui Zhou

Open access · goldAbstract read
In one paragraph

Article in BMC pregnancy and childbirth, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-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

10 citing papers in PubMed, 26 citations in OpenAlex.

  1. Chemokines in Pregnancy.Biomolecules · 2025
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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.

Jiayi ZhengMedical Center for Human Reproduction, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, People's Republic of China.
Danni QuMedical Center for Human Reproduction, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, People's Republic of China.
Chen WangMedical Center for Human Reproduction, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, People's Republic of China.
Ling DingMedical Center for Human Reproduction, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, People's Republic of China.
Wenhui ZhouMedical Center for Human Reproduction, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, People's Republic of China. wenhuizhbjcy@126.com.
Capital Medical University · CNBeijing Chao-Yang Hospital · CN

Funding

National Natural Science Foundation of China 81471511
6 · The paper itself

Abstract

backgroundCXCL12(chemokine ligand 12, CXCL12) and its receptors CXCR4 are widely expressed in maternal-fetal interface and plays an adjust role in materno-fetal dialogue and immune tolerance during early pregnancy. This study aimed to evaluate the role and mechanism of self-derived CXCL12 in modulating the functions of human first-trimester endometrial epithelial cells (EECs) and to identify the potential protein kinase signaling pathways involved in the CXCL12/CXCR4's effect on EECs.

methodsThe expression of CXCL12 and CXCR4 in EECs was measured by using immunohistochemistry, immunofluorescence, real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The effects of EEC-conditioned medium (EEC-CM) and recombinant human CXCL12 (rhCXCL12) on EEC migration and invasion in vitro were evaluated with migration and invasion assays. In-cell western blot analysis was used to examine the phosphorylation of protein kinase B (AKT), extracellular regulated protein kinases (ERKs) and phosphatidylinositol 3-kinase (PI3K) after CXCL12 treatment.

resultsCXCL12 and CXCR4 were both expressed in human first-trimester EECs at the mRNA and protein level. Both EEC-CM and rhCXCL12 significantly increased the migration and invasion of EECs (P < 0.05), which could be blocked by neutralizing antibodies against CXCR4 (P < 0.05) or CXCL12 (P < 0.05), respectively. CXCL12 activated both PI3K/AKT and ERK1/2 signaling and CXCR4 neutralizing antibody effectively reduced CXCL12-induced phosphorylation of AKT and ERK1/2. LY294002, a PI3K-AKT inhibitor, was able to reverse the promotive effect of EEC-CM or rhCXCL12 on EEC migration and invasion.

conclusionsHuman first-trimester EECs promoted their own migration and invasion through the autocrine mechanism with CXCL12/CXCR4 axis involvement by activating PI3K/AKT signaling. This study contributes to a better understanding of the epithelium function mediated by chemokine and chemokine receptor during normal pregnancy.

Indexed as

Autocrine CommunicationCell Culture TechniquesCell MovementChemokine CXCL12EndometriumEpithelial CellsFemaleHumansPhosphatidylinositol 3-KinasePregnancyPregnancy Trimester, FirstProto-Oncogene Proteins c-aktReceptors, CXCR4Signal TransductionChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktReceptors, CXCR4CXCL12/CXCR4Endometrial epithelial cell (EEC)Maternal-fetal interfaceMotilityPhosphorylation

Identifiers

PMID32041571
PMCPMC7011269
OpenAlexW3006164982

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.