Evidence map›Paper›PMID 30015949›Full record

ArticleMolecular medicine reports2018

RBP4 regulates trophoblastic cell proliferation and invasion via the PI3K/AKT signaling pathway.

Hongxia Li, Guangming Cao, Nawei Zhang, Tong Lou, Qiushi Wang, Zhenyu Zhang, Chongdong Liu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Observational
  3. Article
  4. Screening and analysis of plasma differential lncRNA/mRNA in early pregnancy of preeclampsia.Malawi medical journal : the journal of Medical Association of Malawi · 2025
    Article
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  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Role of adipokines in embryo implantation.Endocrine connections · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Novel adipokine associated with OA: retinol binding protein 4 (RBP4) is produced by cartilage and is correlated with MMPs in osteoarthritis patients.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  19. [miR-34a-5p regulates viability, invasion and apoptosis of placental trophoblastic cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    Article
  20. Article
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 2 institutions in 1 country.

Hongxia LiDepartment of Obstetrics and Gynecology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Guangming CaoDepartment of Obstetrics and Gynecology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Nawei ZhangDepartment of Obstetrics and Gynecology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Tong LouDepartment of Obstetrics and Gynecology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Qiushi WangDepartment of Obstetrics and Gynecology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Zhenyu ZhangDepartment of Obstetrics and Gynecology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Chongdong LiuDepartment of Obstetrics and Gynecology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, P.R. China.
Beijing Chao-Yang Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insufficient trophoblast invasion is associated with preeclampsia (PE) development. Retinol-binding protein 4 (RBP4) is important for regulating cell differentiation, migration and invasion. The aim of the present study was to determine RBP4 expression and function in the human placenta and to examine the underlying mechanisms. In the present study, RBP4 expression was determined in serum samples from 35 pregnant women with PE and 30 healthy pregnant women using enzyme-linked immunosorbent assays. Cell proliferation was assessed by Cell Counting Kit-8 assays, and cell invasion was examined with transwell assays. RBP4 concentrations were significantly lower in the PE group when compared with the control group. RBP4 overexpression enhanced HTR8/SVneo cell proliferation and invasion, and the levels of phosphorylated (p-) phosphoinositide 3-kinase (PI3K) and p-protein kinase B (AKT) in HTR8/SVneo cells. RBP4 knockdown significantly inhibited HTR8/SVneo cell proliferation and invasion, and repressed the expression of matrix metalloproteinases. In addition, RBP4 knockdown significantly reduced the levels of p-PI3K and p-AKT in HTR8/SVneo cells. Taken together, the results of the present study demonstrated that RBP4 overexpression increased HTR8/SVneo cell proliferation and invasion by suppressing PI3K/AKT signaling and RBP4 knockdown induced the opposite effects.

Indexed as

Cell ProliferationAdultCell LineCell MovementFemaleGestational AgeHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9Phosphatidylinositol 3-KinasesPlacentaPre-EclampsiaPregnancyProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Retinol-Binding Proteins, PlasmaBCL2 protein, humanMatrix Metalloproteinase 2Matrix Metalloproteinase 9Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2RBP4 protein, humanRetinol-Binding Proteins, PlasmaRNA, Small Interfering

Identifiers

PMID30015949
PMCPMC6102697
OpenAlexW2811487120

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.