Evidence map›Paper›PMID 30298908›Full record

ArticleBiotechnology and bioengineering2019

Trophoblast-endothelium signaling involves angiogenesis and apoptosis in a dynamic bioprinted placenta model.

Che-Ying Kuo, Mariya Shevchuk, Justin Opfermann, Ting Guo, Marco Santoro, John P Fisher, Peter Cw Kim

Abstract read
In one paragraph

Article in Biotechnology and bioengineering, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  20. Engineered Liver Tissue Culture in anTissue engineering. Part A · 2020
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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 2 institutions in 1 country.

Che-Ying KuoFischell Department of Bioengineering, University of Maryland, College Park, Maryland.ORCID 0000-0002-0366-8386
Mariya ShevchukFischell Department of Bioengineering, University of Maryland, College Park, Maryland.
Justin OpfermannPediatric Tissue Engineering and Regenerative Medicine Program, Sheikh Zayed Institute for Pediatric Surgical Innovation, Children's National Health System, Washington, District of Columbia.
Ting GuoFischell Department of Bioengineering, University of Maryland, College Park, Maryland.
Marco SantoroFischell Department of Bioengineering, University of Maryland, College Park, Maryland.ORCID 0000-0003-1914-8921
John P FisherFischell Department of Bioengineering, University of Maryland, College Park, Maryland.
Peter Cw KimPediatric Tissue Engineering and Regenerative Medicine Program, Sheikh Zayed Institute for Pediatric Surgical Innovation, Children's National Health System, Washington, District of Columbia.
Children's National · USUniversity of Maryland, College Park · US

Funding

Training and Dissemination CoreP41EB023833 · NIBIB · UNIV OF MARYLAND, COLLEGE PARK · PI MIKOS, ANTONIOS G. · 2017 to 2021
$6.2M
NIBIB NIH HHS P41 EB023833
6 · The paper itself

Abstract

Trophoblast invasion and remodeling of the maternal spiral arteries are required for pregnancy success. Aberrant endothelium-trophoblast crosstalk may lead to preeclampsia, a pregnancy complication that has serious effects on both the mother and the baby. However, our understanding of the mechanisms involved in this pathology remains elementary because the current in vitro models cannot describe trophoblast-endothelium interactions under dynamic culture. In this study, we developed a dynamic three-dimensional (3D) placenta model by bioprinting trophoblasts and an endothelialized lumen in a perfusion bioreactor. We found the 3D printed perfusion bioreactor system significantly augmented responses of endothelial cells by encouraging network formations and expressions of angiogenic markers, cluster of differentiation 31 (CD31), matrix metalloproteinase-2 (MMP2), matrix metalloproteinase-9 (MMP9), and vascular endothelial growth factor A (VEGFA). Bioprinting favored colocalization of trophoblasts with endothelial cells, similar to in vivo observations. Additional analysis revealed that trophoblasts reduced the angiogenic responses by reducing network formation and motility rates while inducing apoptosis of endothelial cells. Moreover, the presence of endothelial cells appeared to inhibit trophoblast invasion rates. These results clearly demonstrated the utility and potential of bioprinting and perfusion bioreactor system to model trophoblast-endothelium interactions in vitro. Our bioprinted placenta model represents a crucial step to develop advanced research approach that will expand our understanding and treatment options of preeclampsia and other pregnancy-related pathologies.

Indexed as

ApoptosisBioprintingCell CommunicationNeovascularization, PhysiologicSignal TransductionEndothelial CellsHumansModels, TheoreticalTrophoblasts3D Bioprintingbioreactorendotheliumplacentapreeclampsia

Identifiers

PMID30298908
PMCPMC6289739
OpenAlexW2896805781

What OpenQuestion holds

Textmetadata
LicenceTDM
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.