About: Atrial overexpression of angiotensin-converting enzyme 2 improves the canine rapid atrial pacing-induced structural and electrical remodeling: Fan, ACE2 improves atrial substrate remodeling

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About: Atrial overexpression of angiotensin-converting enzyme 2 improves the canine rapid atrial pacing-induced structural and electrical remodeling: Fan, ACE2 improves atrial substrate remodeling Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Atrial overexpression of angiotensin-converting enzyme 2 improves the canine rapid atrial pacing-induced structural and electrical remodeling: Fan, ACE2 improves atrial substrate remodeling
Creator	Zhang, Bo Li, • Chen, Shaojie Cui, Kun Fan, Jinqi Ling, Zhiyu Yin, Yuehui Zhang, Quanjun Zou, Lili Huaan Du, • Kamsang Woo, • Lan, • Zrenner, •
Source	PMC
abstract	The purpose of this study was to investigate whether atrial overexpression of angiotensin-converting enzyme 2 (ACE2) by homogeneous transmural atrial gene transfer can reverse atrial remodeling and its mechanisms in a canine atrial-pacing model. Twenty-eight mongrel dogs were randomly divided into four groups: Sham-operated, AF-control, gene therapy with adenovirus-enhanced green fluorescent protein (Ad-EGFP) and gene therapy with Ad-ACE2 (Ad-ACE2) (n = 7 per subgroup). AF was induced in all dogs except the Sham-operated group by rapid atrial pacing at 450 beats/min for 2 weeks. Ad-EGFP and Ad-ACE2 group then received epicardial gene painting. Three weeks after gene transfer, all animals except the Sham group underwent rapid atrial pacing for another 3 weeks and then invasive electrophysiological, histological and molecular studies. The Ad-ACE2 group showed an increased ACE2 and Angiotensin-(1–7) expression, and decreased Angiotensin II expression in comparison with Ad-EGFP and AF-control group. ACE2 overexpression attenuated rapid atrial pacing-induced increase in activated extracellular signal-regulated kinases and mitogen-activated protein kinases (MAPKs) levels, and decrease in MAPK phosphatase 1(MKP-1) level, resulting in attenuation of atrial fibrosis collagen protein markers and transforming growth factor-β1. Additionally, ACE2 overexpression also modulated the tachypacing-induced up-regulation of connexin 40, down-regulation of connexin 43 and Kv4.2, and significantly decreased the inducibility and duration of AF. ACE2 overexpression could shift the renin–angiotensin system balance towards the protective axis, attenuate cardiac fibrosis remodeling associated with up-regulation of MKP-1 and reduction of MAPKs activities, modulate tachypacing-induced ion channels and connexin remodeling, and subsequently reduce the inducibility and duration of AF. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00395-015-0499-0) contains supplementary material, which is available to authorized users.
has issue date	2015-07-05(xsd:dateTime)
bibo:doi	10.1007/s00395-015-0499-0
bibo:pmid	26143546
has license	no-cc
sha1sum (hex)	c342709015191b6879001fe3661422851bf0ec01
schema:url	https://doi.org/10.1007/s00395-015-0499-0
resource representing a document's title	Atrial overexpression of angiotensin-converting enzyme 2 improves the canine rapid atrial pacing-induced structural and electrical remodeling: Fan, ACE2 improves atrial substrate remodeling
has PubMed Central identifier	PMC7101981
has PubMed identifier	26143546
schema:publication	Basic Res Cardiol
resource representing a document's body	covid:c342709015191b6879001fe3661422851bf0ec01#body_text
is schema:about of	named entity 'MAPKs' named entity 'atrial' named entity 'weeks' named entity 'connexin' named entity 'MKP' named entity 'pacing' named entity 'atrial' named entity 'expression' named entity 'group' named entity 'electrophysiological' named entity 'rapid' named entity 'study' named entity 'gene' named entity 'MKP' named entity 'channels' named entity 'painting' named entity 'attenuation' named entity 'subgroup' named entity 'angiotensin-converting enzyme 2' named entity 'remodeling' named entity 'green fluorescent protein' named entity 'histological' named entity 'ACE2' named entity 'Kv4.2' named entity 'EGFP' named entity 'fibrosis' named entity 'Sham-operated group' named entity 'epicardial' named entity 'ACE2' named entity 'angiotensin-converting enzyme 2' named entity 'down-regulation' named entity 'mitogen-activated protein kinases' named entity 'angiotensin-converting enzyme 2' named entity 'connexin' named entity 'transgenic mice' named entity 'atrial myocytes' named entity 'ACE2' named entity 'ACE' named entity 'ACE2' named entity 'mRNA expression' named entity 'ACE2' named entity 'MAPK phosphatase' named entity 'fibrosis' named entity 'metabolizes' named entity 'CX40' named entity 'IgG' named entity 'AT1R' named entity 'EGFP' named entity 'connexin' named entity 'test-tube' named entity 'EGFP' named entity 'virus' named entity '5.8' named entity 'heptapeptide' named entity 'atrial myocytes' named entity 'EGFP' named entity 'phosphorylation' named entity 'densitometry' named entity 'RNA' named entity 'receptor' named entity 'extracellular signal-regulated kinases' named entity 'gene transfer' named entity 'action potential' named entity 'enzyme-linked immunosorbent assay' named entity 'fibronectin' named entity 'critical role' named entity 'CX43' named entity 'hemodynamic' named entity 'fibrosis'

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