Evidence map›Paper›PMID 41296227›Full record

ArticleAnnals of biomedical engineering2026

Development of a Stereolithography 3D Printing-Based Micropatterning Method to Study Endothelial-to-Mesenchymal Transition Mechanobiology.

Karina Bender, Sarah Chesley, Jay Lesny Drake, Megan Ho, Emily Lin, Kathryn Saxton, Ninava Sharma, Christina K Tripsas, Qian Li, Jeffrey J Hsu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of biomedical engineering, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Karina BenderDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Sarah ChesleyDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Jay Lesny DrakeDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Megan HoDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Emily LinDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Kathryn SaxtonDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Ninava SharmaDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA.
Christina K TripsasDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, David Geffen School of Medicine, Los Angeles, California, USA.
Qian LiDepartment of Medicine, University of California, Los Angeles, Los Angeles, California, USA.
Jeffrey J HsuDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, California, USA. jjhsu@mednet.ucla.edu.ORCID http://orcid.org/0000-0002-9971-5916

Funding

Mechanobiology of Endothelial-to-Mesenchymal Transition in Cardiovascular CalcificationK08HL151961 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HSU, JEFFREY JOHN · 2020 to 2024
$646k
NHLBI NIH HHS K08 HL151961NHLBI NIH HHS K08HL151961
6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndMT) is the process of endothelial cells undergoing molecular changes that shift their phenotype from that of endothelial cells to that of mesenchymal-like cells. It is a crucial developmental process that has been implicated in various physiological and pathological conditions. EndMT has gained attention as a potential therapeutic target for cardiovascular disease processes, including atherosclerosis, myocardial fibrosis, and vascular calcification. In addition to the assessment of endothelial and mesenchymal markers, the behavioral mechanics of endothelial cells, such as migration and invasion, are often used to identify endothelial cells that have undergone EndMT. However, whether cell chirality may be another mechanobiological marker of EndMT remains unclear. In this study, we aimed to develop an accessible micropatterning platform and created a stereolithography (SLA) 3D printing-based polydimethylsiloxane (PDMS) protein-stamp fabrication platform to create customized patterns of ECM proteins to study endothelial cell chirality during EndMT. Human aortic endothelial cells (HAECs) were treated with the inflammatory cytokine tumor necrosis factor-α (TNF-α), which resulted in the downregulation of the endothelial marker ENOS3 and the upregulation of the mesenchymal markers N-cadherin and transgelin, supporting the induction of EndMT. HAECs were seeded onto fibronectin stripe micropatterns, and cell chirality was measured using custom cell-profiling software. HAECs treated with TNF-α exhibited a shift in cell orientation by approximately 18°, supporting altered cell chirality during TNF-α-induced EndMT. Our work innovates novel methods of studying EndMT by developing a flexible and cost-effective protein-stamp fabrication and image analysis pipeline. This pipeline can be used by researchers to study the endothelial cell chirality in response to EndMT induction.

Indexed as

Endothelial CellsEpithelial-Mesenchymal TransitionPrinting, Three-DimensionalAortaDimethylpolysiloxanesHumansDimethylpolysiloxanesAtherosclerosisCell chiralityEndothelial-to-mesenchymal transition (EndMT)MechanobiologyMicropatterning

Identifiers

PMID41296227
PMCPMC12729161

What Socratic holds

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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 Socratic graph.