Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis

Background and aimsThe role of circular RNAs (circRNAs) in the pathophysiology of cardiovascular disease is gradually being elucidated; however, their roles in atrial fibrillation (AF)-related fibrosis are largely unknown. This study aimed to characterize the different circRNA profiles in the rapid-...

Full description

Bibliographic Details
Main Authors: Wenfeng Shangguan, Tianshu Gu, Rukun Cheng, Xing Liu, Yu Liu, Shuai Miao, Weiding Wang, Fang Song, Hualing Wang, Tong Liu, Xue Liang
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-08-01
Series:Frontiers in Cardiovascular Medicine
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcvm.2023.1110707/full
_version_ 1797767517353017344
author Wenfeng Shangguan
Tianshu Gu
Rukun Cheng
Xing Liu
Yu Liu
Shuai Miao
Weiding Wang
Fang Song
Hualing Wang
Tong Liu
Xue Liang
author_facet Wenfeng Shangguan
Tianshu Gu
Rukun Cheng
Xing Liu
Yu Liu
Shuai Miao
Weiding Wang
Fang Song
Hualing Wang
Tong Liu
Xue Liang
author_sort Wenfeng Shangguan
collection DOAJ
description Background and aimsThe role of circular RNAs (circRNAs) in the pathophysiology of cardiovascular disease is gradually being elucidated; however, their roles in atrial fibrillation (AF)-related fibrosis are largely unknown. This study aimed to characterize the different circRNA profiles in the rapid-pacing atria of dogs and explore the mechanisms involved in atrial fibrosis.MethodsA rapid right atrial-pacing model was established using electrical stimulation from a pacemaker. After 14 days, atrial tissue was collected for circRNA sequencing analysis. In vitro fibrosis was established by stimulating canine atrial fibroblasts with angiotensin II (Ang II). The fibroblasts were transfected with siRNA and overexpressing plasmids to explore the effects of cfa-circ002203 on fibroblast proliferation, migration, differentiation, and the expression of fibrosis-related proteins.ResultsIn total, 146 differentially expressed circRNAs were screened, of which 106 were upregulated and 40 were downregulated. qRT-PCR analysis showed that cfa-circ002203 was upregulated in both in vivo and in vitro fibroblast fibrosis models. The upregulation of cfa-circ002203 enhanced proliferation and migration while weakening the apoptosis of fibroblasts. Western blotting showed that cfa-circ002203 overexpression increased the protein expression levels of fibrosis-related indicators (Col I, Col III, MMP2, MMP9, and α-SMA) and decreased the protein expression levels of pro-apoptotic factors (Bax and Caspase 3) in Ang II-induced fibroblast fibrosis.ConclusionCfa-circ002203 might serve as an active promoter of the proliferation, migration, and fibrosis of atrial fibroblasts and is involved in AF-induced fibroblast fibrosis.
first_indexed 2024-03-12T20:40:57Z
format Article
id doaj.art-3c69b950c8ca46d4a4244b9c2271ca15
institution Directory Open Access Journal
issn 2297-055X
language English
last_indexed 2024-03-12T20:40:57Z
publishDate 2023-08-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Cardiovascular Medicine
spelling doaj.art-3c69b950c8ca46d4a4244b9c2271ca152023-08-01T08:47:48ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2023-08-011010.3389/fcvm.2023.11107071110707Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosisWenfeng Shangguan0Tianshu Gu1Rukun Cheng2Xing Liu3Yu Liu4Shuai Miao5Weiding Wang6Fang Song7Hualing Wang8Tong Liu9Xue Liang10Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaDepartment of Cardiology, Taikang Ningbo Hospital, Ningbo, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaDepartment of Geriatric, The Second Hospital of Tianjin Medical University, Tianjin, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, ChinaBackground and aimsThe role of circular RNAs (circRNAs) in the pathophysiology of cardiovascular disease is gradually being elucidated; however, their roles in atrial fibrillation (AF)-related fibrosis are largely unknown. This study aimed to characterize the different circRNA profiles in the rapid-pacing atria of dogs and explore the mechanisms involved in atrial fibrosis.MethodsA rapid right atrial-pacing model was established using electrical stimulation from a pacemaker. After 14 days, atrial tissue was collected for circRNA sequencing analysis. In vitro fibrosis was established by stimulating canine atrial fibroblasts with angiotensin II (Ang II). The fibroblasts were transfected with siRNA and overexpressing plasmids to explore the effects of cfa-circ002203 on fibroblast proliferation, migration, differentiation, and the expression of fibrosis-related proteins.ResultsIn total, 146 differentially expressed circRNAs were screened, of which 106 were upregulated and 40 were downregulated. qRT-PCR analysis showed that cfa-circ002203 was upregulated in both in vivo and in vitro fibroblast fibrosis models. The upregulation of cfa-circ002203 enhanced proliferation and migration while weakening the apoptosis of fibroblasts. Western blotting showed that cfa-circ002203 overexpression increased the protein expression levels of fibrosis-related indicators (Col I, Col III, MMP2, MMP9, and α-SMA) and decreased the protein expression levels of pro-apoptotic factors (Bax and Caspase 3) in Ang II-induced fibroblast fibrosis.ConclusionCfa-circ002203 might serve as an active promoter of the proliferation, migration, and fibrosis of atrial fibroblasts and is involved in AF-induced fibroblast fibrosis.https://www.frontiersin.org/articles/10.3389/fcvm.2023.1110707/fullatrial fibrillationatrial fibrosishigh-throughput sequencingbioinformaticscfa-circ002203
spellingShingle Wenfeng Shangguan
Tianshu Gu
Rukun Cheng
Xing Liu
Yu Liu
Shuai Miao
Weiding Wang
Fang Song
Hualing Wang
Tong Liu
Xue Liang
Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis
Frontiers in Cardiovascular Medicine
atrial fibrillation
atrial fibrosis
high-throughput sequencing
bioinformatics
cfa-circ002203
title Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis
title_full Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis
title_fullStr Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis
title_full_unstemmed Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis
title_short Cfa-circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis
title_sort cfa circ002203 was upregulated in rapidly paced atria of dogs and involved in the mechanisms of atrial fibrosis
topic atrial fibrillation
atrial fibrosis
high-throughput sequencing
bioinformatics
cfa-circ002203
url https://www.frontiersin.org/articles/10.3389/fcvm.2023.1110707/full
work_keys_str_mv AT wenfengshangguan cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT tianshugu cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT rukuncheng cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT xingliu cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT yuliu cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT shuaimiao cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT weidingwang cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT fangsong cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT hualingwang cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT tongliu cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis
AT xueliang cfacirc002203wasupregulatedinrapidlypacedatriaofdogsandinvolvedinthemechanismsofatrialfibrosis