Evidence map›Paper›PMID 38435791›Full record

ArticleCellular and molecular bioengineering2024

Trisomy 21 Alters Cell Proliferation and Migration of iPSC-Derived Cardiomyocytes on Type VI Collagen.

Rachel S Reeser, Alyssa K Salazar, Kendra M Prutton, James R Roede, Mitchell C VeDepo, Jeffrey G Jacot

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular bioengineering, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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

6 authors at 4 institutions in 1 country.

Rachel S ReeserDepartment of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO 80045 USA.
Alyssa K SalazarDepartment of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO 80045 USA.
Kendra M PruttonLinda Crnic Institute for Down Syndrome, Colorado, Aurora, CO 80045 USA.
James R RoedeLinda Crnic Institute for Down Syndrome, Colorado, Aurora, CO 80045 USA.
Mitchell C VeDepoDepartment of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO 80045 USA.
Jeffrey G JacotDepartment of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO 80045 USA.ORCID 0000-0002-1272-5055
Rome Foundation · USChildren's Hospital Colorado · USPennsylvania State University · USUniversity of Colorado Anschutz Medical Campus · US

Funding

Xenobiotic Biotransformation in Down SyndromeR01ES027593 · NIEHS · UNIVERSITY OF COLORADO DENVER · PI James R Roede · 2017 to 2026
$5.1M
Cardiovascular Biomechanics and Imaging in Down SyndromeT32HL072738 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI SHANDAS, ROBIN · 2003 to 2025
$4.9M
PRE-VASCULARIZED AND DEGRADABLE PATCHES FOR CORRECTION OF CONGENITAL HEART DEFECTSR01HL130436 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI JACOT, JEFFREY G · 2016 to 2020
$2.0M
NHLBI NIH HHS R01 HL130436NHLBI NIH HHS T32 HL072738NIEHS NIH HHS R01 ES027593
6 · The paper itself

Abstract

Purpose: Individuals with Down syndrome (DS) are 2000 times more likely to develop a congenital heart defect (CHD) than the typical population Freeman et al. in Am J Med Genet 80:213-217 (1998). The majority of CHDs in individuals with DS characteristically involve the atrioventricular (AV) canal, including the valves and the atrial or ventricular septum. Type VI collagen (COLVI) is the primary structural component in the developing septa and endocardial cushions, with two of the three genes encoding for COLVI located on human chromosome 21 and upregulated in Down syndrome (von Kaisenberg et al. in Obstet Gynecol 91:319-323, 1998; Gittenberger-De Groot et al. in Anatom Rec Part A 275:1109-1116, 2023). Methods: To investigate the effect of COLVI dosage on cardiomyocytes with trisomy 21, induced pluripotent stem cells (iPSC) from individuals with DS and age- and sex-matched controls were differentiated into cardiomyocytes (iPSC-CM) and plated on varying concentrations of COLVI. Results: Real time quantitative PCR showed decreased expression of cardiac-specific genes of DS iPSC-CM lines compared to control iPSC-CM. As expected, DS iPSC-CM had increased expression of genes on chromosome 21, including Conclusions: These results suggest that the increased expression of COLVI in DS may result in lower migration-driven elongation of endocardial cushions stemming from lower cell proliferation and migration, possibly contributing to the high incidence of CHD in the DS population. Supplementary Information: The online version contains supplementary material available at 10.1007/s12195-023-00791-x.

Indexed as

Congenital heart defectsDown syndromeEndocardial cushionsExtracellular matrixHeart development

Identifiers

PMID38435791
PMCPMC10901762
OpenAlexW4390571872

What OpenQuestion holds

Textmetadata
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.