Evidence map›Paper›PMID 29986945›Full record

ArticleCirculation research2018

Large-Scale Single-Cell RNA-Seq Reveals Molecular Signatures of Heterogeneous Populations of Human Induced Pluripotent Stem Cell-Derived Endothelial Cells.

David T Paik, Lei Tian, Jaecheol Lee, Nazish Sayed, Ian Y Chen, Siyeon Rhee, June-Wha Rhee, Youngkyun Kim, Robert C Wirka, Jan W Buikema and 4 more

Abstract read
In one paragraph

Article in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing 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

101 citing papers in PubMed.

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41 more citing papers are in PubMed but not listed here.

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

14 authors.

David T PaikFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Lei TianFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Jaecheol LeeFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Nazish SayedFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Ian Y ChenFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Siyeon RheeDepartment of Biology, Stanford University, CA (S.R., K.R.-H.).
June-Wha RheeFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Youngkyun KimFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Robert C WirkaFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Jan W BuikemaFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Sean M WuFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Kristy Red-HorseFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Thomas QuertermousFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).
Joseph C WuFrom the Stanford Cardiovascular Institute, CA (D.T.P., L.T., J.L., N.S., I.Y.C., J.-W.R., Y.K., R.C.W., J.W.B., S.M.W., K.R.-H., T.Q., J.C.W.).

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
Elucidating Mechanism of Cardiac Fibrosis with Cell Village of Pooled Human iPSCsR01HL130020 · NHLBI · STANFORD UNIVERSITY · PI Ronglih Liao, MARK MERCOLA · 2016 to 2026
$7.3M
Human Induced Pluripotent Stem Cells for Cardiovascular Disease ModelingR01HL113006 · NHLBI · STANFORD UNIVERSITY · PI WU, JOSEPH C. · 2012 to 2025
$6.8M
T32 Training Program in Mechanisms and Innovation in Vascular DiseaseT32HL098049 · NHLBI · STANFORD UNIVERSITY · PI Nicholas James Leeper, Philip S Tsao · 2010 to 2026
$6.3M
Causal variant association mechanisms in TCF21 binding coronary disease lociR01HL134817 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2017 to 2026
$6.2M
Mechanism of the Coronary Heart Disease Association at Chromosome 6q23.2R01HL109512 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2011 to 2019
$6.1M
Mechanotransduction and transcriptional regulation during artery developmentR01HL128503 · NHLBI · STANFORD UNIVERSITY · PI Mary Red-Horse · 2015 to 2026
$5.8M
Modeling Susceptibility to Chemotherapy-Induced Cardiotoxicity Using Human iPSCsR01HL123968 · NHLBI · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS, WU, JOSEPH C. · 2014 to 2021
$4.8M
Multi-Disciplinary Training Program in Cardiovascular Imaging at StanfordT32EB009035 · NIBIB · STANFORD UNIVERSITY · PI Koen Nieman, John M. Pauly · 2008 to 2026
$4.3M
The SMAD3 signaling network in coronary artery disease riskR01HL139478 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2018 to 2026
$3.7M
A Systems Biology Approach to Study Cardiac Arrhythmias: iPS Cells and In Silico ModelingR01HL128170 · NHLBI · STANFORD UNIVERSITY · PI ALTMAN, RUSS BIAGIO, CLANCY, COLLEEN E · 2015 to 2018
$3.0M
Assessment of Low-Dose Radiation Risk and Mechanisms of Individual RadiosensitivityR01HL132875 · NHLBI · STANFORD UNIVERSITY · PI WU, JOSEPH C. · 2016 to 2019
$1.9M
American Heart Association-American Stroke Association 13SDG17340025NHLBI NIH HHS F32 HL134221NHLBI NIH HHS K01 HL135455NHLBI NIH HHS R01 HL109512NHLBI NIH HHS R01 HL113006NHLBI NIH HHS R01 HL123968NHLBI NIH HHS R01 HL128170NHLBI NIH HHS R01 HL128503NHLBI NIH HHS R01 HL130020NHLBI NIH HHS R01 HL132875NHLBI NIH HHS R01 HL134817NHLBI NIH HHS R01 HL139478NHLBI NIH HHS R33 HL120757NIBIB NIH HHS T32 EB009035NIDDK NIH HHS P30 DK116074
6 · The paper itself

Abstract

rationaleHuman-induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) have risen as a useful tool in cardiovascular research, offering a wide gamut of translational and clinical applications. However, inefficiency of the currently available iPSC-EC differentiation protocol and underlying heterogeneity of derived iPSC-ECs remain as major limitations of iPSC-EC technology.

objectiveHere, we performed droplet-based single-cell RNA sequencing (scRNA-seq) of the human iPSCs after iPSC-EC differentiation. Droplet-based scRNA-seq enables analysis of thousands of cells in parallel, allowing comprehensive analysis of transcriptional heterogeneity. METHODS AND

resultsBona fide iPSC-EC cluster was identified by scRNA-seq, which expressed high levels of endothelial-specific genes. iPSC-ECs, sorted by CD144 antibody-conjugated magnetic sorting, exhibited standard endothelial morphology and function including tube formation, response to inflammatory signals, and production of NO. Nonendothelial cell populations resulting from the differentiation protocol were identified, which included immature cardiomyocytes, hepatic-like cells, and vascular smooth muscle cells. Furthermore, scRNA-seq analysis of purified iPSC-ECs revealed transcriptional heterogeneity with 4 major subpopulations, marked by robust enrichment of CLDN5, APLNR, GJA5, and ESM1 genes, respectively.

conclusionsMassively parallel, droplet-based scRNA-seq allowed meticulous analysis of thousands of human iPSCs subjected to iPSC-EC differentiation. Results showed inefficiency of the differentiation technique, which can be improved with further studies based on identification of molecular signatures that inhibit expansion of nonendothelial cell types. Subtypes of bona fide human iPSC-ECs were also identified, allowing us to sort for iPSC-ECs with specific biological function and identity.

Indexed as

TranscriptomeApelin ReceptorsCell DifferentiationCells, CulturedClaudin-5ConnexinsEndothelial CellsGap Junction alpha-5 ProteinHumansInduced Pluripotent Stem CellsNeoplasm ProteinsProteoglycansSingle-Cell AnalysisApelin ReceptorsAPLNR protein, humanClaudin-5CLDN5 protein, humanConnexinsESM1 protein, humanGap Junction alpha-5 ProteinNeoplasm ProteinsProteoglycanscomputational biologyendothelial cellsinduced pluripotent stem cellsmyocytes, cardiacstem cells

Identifiers

PMID29986945
PMCPMC6202208

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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.