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Article: Modulation of chromatin remodeling proteins SMYD1 and SMARCD1 promotes contractile function of human pluripotent stem cell-derived ventricular cardiomyocyte in 3D-engineered cardiac tissues

TitleModulation of chromatin remodeling proteins SMYD1 and SMARCD1 promotes contractile function of human pluripotent stem cell-derived ventricular cardiomyocyte in 3D-engineered cardiac tissues
Authors
KeywordsMyocytes, Cardiac
Induced Pluripotent Stem Cells
Cardiomyocytes CMs
Issue Date2019
PublisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html
Citation
Scientific Reports, 2019, v. 9, p. article no. 7502 How to Cite?
AbstractHuman embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) have the ability of differentiating into functional cardiomyocytes (CMs) for cell replacement therapy, tissue engineering, drug discovery and toxicity screening. From a scale-free, co-expression network analysis of transcriptomic data that distinguished gene expression profiles of undifferentiated hESC, hESC-, fetal- and adult-ventricular(V) CM, two candidate chromatin remodeling proteins, SMYD1 and SMARCD1 were found to be differentially expressed. Using lentiviral transduction, SMYD1 and SMARCD1 were over-expressed and suppressed, respectively, in single hESC-VCMs as well as the 3D constructs Cardiac Micro Tissues (CMT) and Tissue Strips (CTS) to mirror the endogenous patterns, followed by dissection of their roles in controlling cardiac gene expression, contractility, Ca2+-handling, electrophysiological functions and in vitro maturation. Interestingly, compared to independent single transductions, simultaneous SMYD1 overexpression and SMARCD1 suppression in hESC-VCMs synergistically interacted to increase the contractile forces of CMTs and CTSs with up-regulated transcripts for cardiac contractile, Ca2+-handing, and ion channel proteins. Certain effects that were not detected at the single-cell level could be unleashed under 3D environments. The two chromatin remodelers SMYD1 and SMARCD1 play distinct roles in cardiac development and maturation, consistent with the notion that epigenetic priming requires triggering signals such as 3D environmental cues for pro-maturation effects.
Persistent Identifierhttp://hdl.handle.net/10722/277184
ISSN
2017 Impact Factor: 4.122
2015 SCImago Journal Rankings: 2.073
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorChow, MZY-
dc.contributor.authorSadrian, SN-
dc.contributor.authorKeung, W-
dc.contributor.authorGeng, L-
dc.contributor.authorRen, L-
dc.contributor.authorKong, CW-
dc.contributor.authorWong, AOT-
dc.contributor.authorHulot, JS-
dc.contributor.authorChen, CS-
dc.contributor.authorCosta, KD-
dc.contributor.authorHajjar, RJ-
dc.contributor.authorLi, RA-
dc.date.accessioned2019-09-20T08:46:13Z-
dc.date.available2019-09-20T08:46:13Z-
dc.date.issued2019-
dc.identifier.citationScientific Reports, 2019, v. 9, p. article no. 7502-
dc.identifier.issn2045-2322-
dc.identifier.urihttp://hdl.handle.net/10722/277184-
dc.description.abstractHuman embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) have the ability of differentiating into functional cardiomyocytes (CMs) for cell replacement therapy, tissue engineering, drug discovery and toxicity screening. From a scale-free, co-expression network analysis of transcriptomic data that distinguished gene expression profiles of undifferentiated hESC, hESC-, fetal- and adult-ventricular(V) CM, two candidate chromatin remodeling proteins, SMYD1 and SMARCD1 were found to be differentially expressed. Using lentiviral transduction, SMYD1 and SMARCD1 were over-expressed and suppressed, respectively, in single hESC-VCMs as well as the 3D constructs Cardiac Micro Tissues (CMT) and Tissue Strips (CTS) to mirror the endogenous patterns, followed by dissection of their roles in controlling cardiac gene expression, contractility, Ca2+-handling, electrophysiological functions and in vitro maturation. Interestingly, compared to independent single transductions, simultaneous SMYD1 overexpression and SMARCD1 suppression in hESC-VCMs synergistically interacted to increase the contractile forces of CMTs and CTSs with up-regulated transcripts for cardiac contractile, Ca2+-handing, and ion channel proteins. Certain effects that were not detected at the single-cell level could be unleashed under 3D environments. The two chromatin remodelers SMYD1 and SMARCD1 play distinct roles in cardiac development and maturation, consistent with the notion that epigenetic priming requires triggering signals such as 3D environmental cues for pro-maturation effects.-
dc.languageeng-
dc.publisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html-
dc.relation.ispartofScientific Reports-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectMyocytes, Cardiac-
dc.subjectInduced Pluripotent Stem Cells-
dc.subjectCardiomyocytes CMs-
dc.titleModulation of chromatin remodeling proteins SMYD1 and SMARCD1 promotes contractile function of human pluripotent stem cell-derived ventricular cardiomyocyte in 3D-engineered cardiac tissues-
dc.typeArticle-
dc.identifier.emailKeung, W: wkeung@hku.hk-
dc.identifier.emailGeng, L: genglin@hku.hk-
dc.identifier.emailLi, RA: ronaldli@hkucc.hku.hk-
dc.identifier.authorityKeung, W=rp01887-
dc.identifier.authorityKong, CW=rp01563-
dc.identifier.authorityLi, RA=rp01352-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41598-019-42953-w-
dc.identifier.pmid31097748-
dc.identifier.pmcidPMC6522495-
dc.identifier.scopuseid_2-s2.0-85065828028-
dc.identifier.hkuros305871-
dc.identifier.volume9-
dc.identifier.spagearticle no. 7502-
dc.identifier.epagearticle no. 7502-
dc.publisher.placeUnited Kingdom-

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