Advanced Single-Cell Mapping Reveals that in hESC Cardiomyocytes Contraction Kinetics and Action Potential Are Independent of Myosin Isoform.
MYH6
MYH7
action potential
cardiac myosin heavy chain
human embryonic stem cell-derived cardiomyocytes
maturation
single-cell mapping technique
twitch contractions
Journal
Stem cell reports
ISSN: 2213-6711
Titre abrégé: Stem Cell Reports
Pays: United States
ID NLM: 101611300
Informations de publication
Date de publication:
12 05 2020
12 05 2020
Historique:
received:
20
12
2018
revised:
12
03
2020
accepted:
17
03
2020
pubmed:
18
4
2020
medline:
17
4
2021
entrez:
18
4
2020
Statut:
ppublish
Résumé
Human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) represent an attractive model to investigate CM function and disease mechanisms. One characteristic marker of ventricular specificity of human CMs is expression of the ventricular, slow β-myosin heavy chain (MyHC), as opposed to the atrial, fast α-MyHC. The main aim of this study was to investigate at the single-cell level whether contraction kinetics and electrical activity of hESC-CMs are influenced by the relative expression of α-MyHC versus β-MyHC. For effective assignment of functional parameters to the expression of both MyHC isoforms at protein and mRNA levels in the very same hESC-CMs, we developed a single-cell mapping technique. Surprisingly, α- versus β-MyHC was not related to specific contractile or electrophysiological properties of the same cells. The multiparametric cell-by-cell analysis suggests that in hESC-CMs the expression of genes associated with electrical activity, contraction, calcium handling, and MyHCs is independently regulated.
Identifiants
pubmed: 32302556
pii: S2213-6711(20)30105-3
doi: 10.1016/j.stemcr.2020.03.015
pmc: PMC7220955
pii:
doi:
Substances chimiques
MYH6 protein, human
0
MYH7 protein, human
0
Protein Isoforms
0
Cardiac Myosins
EC 3.6.1.-
Myosin Heavy Chains
EC 3.6.4.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
788-802Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
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