The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes

10 páginas

Autores:
Rosales, Wendy
Lizcano, Fernando
Tipo de recurso:
Fecha de publicación:
2018
Institución:
Universidad de la Sabana
Repositorio:
Repositorio Universidad de la Sabana
Idioma:
eng
OAI Identifier:
oai:intellectum.unisabana.edu.co:10818/45535
Acceso en línea:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811633/
http://hdl.handle.net/10818/45535
Palabra clave:
hiPSCs
Cardiomyocytes
JMJD2A
ET-1
Cardiac hypertrophy
Rights
License
Attribution-NonCommercial-NoDerivatives 4.0 International
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network_acronym_str REPOUSABA2
network_name_str Repositorio Universidad de la Sabana
repository_id_str
spelling Rosales, WendyLizcano, Fernando11/30/2020 9:232020-11-30T14:23:14Z2018-02-091664-8021https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811633/http://hdl.handle.net/10818/4553510.3389/fgene.2018.0001410 páginasThe development of cardiovascular pathologies is partly attributed to epigenetic causes, including histone methylation, which appears to be an important marker in hearts that develop cardiac hypertrophy. Previous studies showed that the histone demethylase JMJD2A can regulate the hypertrophic process in murine cardiomyocytes. However, the influence of JMJD2A on cardiac hypertrophy in a human cardiomyocyte model is still poorly understood. In the present study, cardiomyocytes derived from human induced pluripotent stem cells (iPSCs) were used. Hypertrophy was induced by angiotensin II and endothelin-1 (ET-1), and transfections were performed to overexpress JMJD2A and for small interfering RNA (siRNA)-induced silencing of JMJD2A. Gene expression analyses were determined using RT-PCR and Western blot. The expression levels of B-type natriuretic peptide (BNP), natriuretic peptide A (ANP), and beta myosin heavy chain (β-MHC) were increased by nearly 2–10-fold with ET-1 compared with the control. However, a higher level of JMJD2A and UTX was detected, whereas the level of JMJD2C was lower. When cardiomyocytes were transiently transfected with JMJD2A, an increase close to 150% in BNP was observed, and this increase was greater after treatment with ET-1. To verify the specificity of JMJD2A activity, a knockdown was performed by means of siRNA-JMJD2A, which led to a significant reduction in BNP. The involvement of JMJD2A suggests that histone-specific modifications are associated with genes encoding proteins that are actively transcribed during the hypertrophy process. Since BNP is closely related to JMJD2A expression, we suggest that there could be a direct influence of JMJD2A on the expression of BNP. These results may be studied further to reduce cardiac hypertrophy via the regulation of epigenetic modifiers.application/pdfengFrontiers in GeneticsFront Genet. 2018; 9: 14Attribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/http://purl.org/coar/access_right/c_abf2Universidad de La SabanaIntellectum Repositorio Universidad de La SabanahiPSCsCardiomyocytesJMJD2AET-1Cardiac hypertrophyThe Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived CardiomyocytesarticlepublishedVersionhttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_6501LICENSElicense.txtlicense.txttext/plain; charset=utf-8498https://intellectum.unisabana.edu.co/bitstream/10818/45535/3/license.txtf52a2cfd4df262e08e9b300d62c85cabMD53CC-LICENSElicense_rdflicense_rdfapplication/rdf+xml; charset=utf-8805https://intellectum.unisabana.edu.co/bitstream/10818/45535/2/license_rdf4460e5956bc1d1639be9ae6146a50347MD5210818/45535oai:intellectum.unisabana.edu.co:10818/455352022-05-10 05:22:19.951Intellectum Universidad de la Sabanacontactointellectum@unisabana.edu.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
dc.title.es_CO.fl_str_mv The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
title The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
spellingShingle The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
hiPSCs
Cardiomyocytes
JMJD2A
ET-1
Cardiac hypertrophy
title_short The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
title_full The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
title_fullStr The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
title_full_unstemmed The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
title_sort The Histone Demethylase JMJD2A Modulates the Induction of Hypertrophy Markers in iPSC-Derived Cardiomyocytes
dc.creator.fl_str_mv Rosales, Wendy
Lizcano, Fernando
dc.contributor.author.none.fl_str_mv Rosales, Wendy
Lizcano, Fernando
dc.subject.es_CO.fl_str_mv hiPSCs
Cardiomyocytes
JMJD2A
ET-1
Cardiac hypertrophy
topic hiPSCs
Cardiomyocytes
JMJD2A
ET-1
Cardiac hypertrophy
description 10 páginas
publishDate 2018
dc.date.accessioned.none.fl_str_mv 11/30/2020 9:23
dc.date.issued.none.fl_str_mv 2018-02-09
dc.date.available.none.fl_str_mv 2020-11-30T14:23:14Z
dc.type.en.fl_str_mv article
dc.type.coarversion.fl_str_mv http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.coar.fl_str_mv http://purl.org/coar/resource_type/c_6501
dc.type.hasVersion.es_CO.fl_str_mv publishedVersion
dc.identifier.issn.none.fl_str_mv 1664-8021
dc.identifier.other.none.fl_str_mv https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811633/
dc.identifier.uri.none.fl_str_mv http://hdl.handle.net/10818/45535
dc.identifier.doi.none.fl_str_mv 10.3389/fgene.2018.00014
identifier_str_mv 1664-8021
10.3389/fgene.2018.00014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811633/
http://hdl.handle.net/10818/45535
dc.language.iso.es_CO.fl_str_mv eng
language eng
dc.relation.ispartofseries.none.fl_str_mv Front Genet. 2018; 9: 14
dc.rights.*.fl_str_mv Attribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.coar.fl_str_mv http://purl.org/coar/access_right/c_abf2
dc.rights.uri.*.fl_str_mv http://creativecommons.org/licenses/by-nc-nd/4.0/
rights_invalid_str_mv Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
http://purl.org/coar/access_right/c_abf2
dc.format.es_CO.fl_str_mv application/pdf
dc.publisher.es_CO.fl_str_mv Frontiers in Genetics
dc.source.es_CO.fl_str_mv Universidad de La Sabana
Intellectum Repositorio Universidad de La Sabana
institution Universidad de la Sabana
bitstream.url.fl_str_mv https://intellectum.unisabana.edu.co/bitstream/10818/45535/3/license.txt
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