Evidence map›Paper›PMID 36652019›Full record

ArticleCellular and molecular life sciences : CMLS2023

A placenta-on-a-chip model to determine the regulation of FKBPL and galectin-3 in preeclampsia.

Sahar Masoumeh Ghorbanpour, Claire Richards, Dillan Pienaar, Kimberly Sesperez, Hamidreza Aboulkheyr Es, Valentina N Nikolic, Natasa Karadzov Orlic, Zeljko Mikovic, Milan Stefanovic, Zoran Cakic and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
13.3field-weighted citation impact, top 1% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Therapeutic Interventions for Preeclampsia: Integrating Placental and Maternal Perspectives.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Review
  5. Review
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  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Evaluating oxidative stress targeting treatments inFrontiers in cell and developmental biology · 2025
    Article
  15. Article
  16. Review
  17. Article
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  19. Article
  20. The Application of Engineered Nanomaterials in Perinatal Therapeutics.Small (Weinheim an der Bergstrasse, Germany) · 2024
    Review
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

17 authors at 5 institutions in 3 countries.

Sahar Masoumeh Ghorbanpour *School of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Claire Richards *School of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Dillan PienaarSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Kimberly SesperezSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Hamidreza Aboulkheyr EsSchool of Biomedical Engineering, Faculty of Engineering and Information Technology, University of Technology Sydney, Sydney, NSW, Australia.
Valentina N NikolicDepartment of Pharmacology and Toxicology, Faculty of Medicine, University of Nis, Niš, Serbia.
Natasa Karadzov OrlicDepartment of Gynaecology and Obstetrics, Narodni Front, Belgrade, Serbia.
Zeljko MikovicDepartment of Gynaecology and Obstetrics, Narodni Front, Belgrade, Serbia.
Milan StefanovicDepartment of Internal Medicine-Gynaecology, Faculty of Medicine, University of Nis, Niš, Serbia.
Zoran CakicDepartment of Gynaecology and Obstetrics, General Hospital of Leskovac, Leskovac, Serbia.
Abdelrahim AlqudahDepartment of Clinical Pharmacy and Pharmacy Practice, Faculty of Pharmaceutical Sciences, The Hashemite University, Zarqa, Jordan.
Louise ColeAustralian Institute of Microbiology and Infection, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Catherine GorrieSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Kristine McGrathSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Mary M KavurmaHeart Research Institute,The University of Sydney, Sydney, NSW, Australia.
Majid Ebrahimi WarkianiInstitute for Biomedical Materials and Devices, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia.
Lana McClementsSchool of Life Sciences, Faculty of Science, University of Technology Sydney, Sydney, NSW, Australia. lana.mcclements@uts.edu.au.ORCID http://orcid.org/0000-0002-4911-1014
University of Technology Sydney · AUUniversity of Belgrade · RSUniversity of Nis · RSHashemite University · JOThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preeclampsia is a pregnancy-specific cardiovascular disorder, involving significant maternal endothelial dysfunction. Although inappropriate placentation due to aberrant angiogenesis, inflammation and shallow trophoblast invasion are the root causes of preeclampsia, pathogenic mechanisms are poorly understood, particularly in early pregnancy. Here, we first confirm the abnormal expression of important vascular and inflammatory proteins, FK506-binding protein-like (FKBPL) and galectin-3 (Gal-3), in human plasma and placental tissues from women with preeclampsia and normotensive controls. We then employ a three-dimensional microfluidic placental model incorporating human umbilical vein endothelial cells (HUVECs) and a first trimester trophoblast cell line (ACH-3P) to investigate FKBPL and Gal-3 signaling in inflammatory conditions. In human samples, both circulating (n = 17 controls; n = 30 preeclampsia) and placental (n ≥ 6) FKBPL and Gal-3 levels were increased in preeclampsia compared to controls (plasma: FKBPL, p < 0.0001; Gal-3, p < 0.01; placenta: FKBPL, p < 0.05; Gal-3, p < 0.01), indicative of vascular dysfunction in preeclampsia. In our placenta-on-a-chip model, we show that endothelial cells are critical for trophoblast-mediated migration and that trophoblasts effectively remodel endothelial vascular networks. Inflammatory cytokine tumour necrosis factor-α (10 ng/mL) modulates both FKBPL and Gal-3 signaling in conjunction with trophoblast migration and impairs vascular network formation (p < 0.005). Our placenta-on-a-chip recapitulates aspects of inappropriate placental development and vascular dysfunction in preeclampsia.

Indexed as

PlacentaPre-EclampsiaCell Cycle ProteinsFemaleGalectin 3HumansHuman Umbilical Vein Endothelial CellsLab-On-A-Chip DevicesPregnancyTacrolimus Binding ProteinsTrophoblastsCell Cycle ProteinsFKBPL protein, humanGalectin 3Tacrolimus Binding ProteinsFKBPLGalectin-3MicrofluidicsPlacental developmentPreeclampsiaVascular remodeling

Identifiers

PMID36652019
PMCPMC9849194
OpenAlexW4317359046

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.