Identification of the optimal reference genes for atrial fibrillation model established by iPSC-derived atrial myocytes.

Atrial fibrillation Atrial fibrillation model Electrical stimulation Induced pluripotent stem cells Quantitative real-time polymerase chain reaction Reference gene

Journal

BMC genomics
ISSN: 1471-2164
Titre abrégé: BMC Genomics
Pays: England
ID NLM: 100965258

Informations de publication

Date de publication:
25 Oct 2024
Historique:
received: 18 05 2024
accepted: 18 10 2024
medline: 26 10 2024
pubmed: 26 10 2024
entrez: 25 10 2024
Statut: epublish

Résumé

Atrial fibrillation (AF) stands as a prevalent and detrimental arrhythmic disorder, characterized by intricate pathophysiological mechanisms. The availability of reliable and reproducible AF models is pivotal in unraveling the underlying mechanisms of this complex condition. Unfortunately, the researchers are still confronted with the absence of consistent in vitro AF models, hindering progress in this crucial area of research. Human induced pluripotent stem cells derived atrial myocytes (hiPSC-AMs) were generated based on the GiWi methods and were verified by whole-cell patch clamp, immunofluorescent staining, and flow cytometry. Then hiPSC-AMs were employed to establish the AF model by HS. Whole-cell patch clamp technique and calcium imaging were used to identify the AF model. The stability of 29 reference genes was evaluated using delta-Ct, GeNorm, NormFinder, and BestKeeper algorithms; RESULTS: HiPSC-AMs displayed atrial myocyte action potentials and expressed the atrial-specific protein MLC-2 A and NR2F2, about 70% of the cardiomyocytes were MLC-2 A positive. After HS, hiPSC-AMs showed a significant increase in beating frequency, a shortened action potential duration, and increased calcium transient frequency. Of the 29 candidate genes, the top five most stably ranked genes were ABL1, RPL37A, POP4, RPL30, and EIF2B1. After normalization using ABL1, KCNJ2 was significantly upregulated in the AF model; Conclusions: In the hiPSC-AMs AF model established by HS, ABL1 provides greater normalization efficiency than commonly used GAPDH.

Sections du résumé

BACKGROUND BACKGROUND
Atrial fibrillation (AF) stands as a prevalent and detrimental arrhythmic disorder, characterized by intricate pathophysiological mechanisms. The availability of reliable and reproducible AF models is pivotal in unraveling the underlying mechanisms of this complex condition. Unfortunately, the researchers are still confronted with the absence of consistent in vitro AF models, hindering progress in this crucial area of research.
METHODS METHODS
Human induced pluripotent stem cells derived atrial myocytes (hiPSC-AMs) were generated based on the GiWi methods and were verified by whole-cell patch clamp, immunofluorescent staining, and flow cytometry. Then hiPSC-AMs were employed to establish the AF model by HS. Whole-cell patch clamp technique and calcium imaging were used to identify the AF model. The stability of 29 reference genes was evaluated using delta-Ct, GeNorm, NormFinder, and BestKeeper algorithms; RESULTS: HiPSC-AMs displayed atrial myocyte action potentials and expressed the atrial-specific protein MLC-2 A and NR2F2, about 70% of the cardiomyocytes were MLC-2 A positive. After HS, hiPSC-AMs showed a significant increase in beating frequency, a shortened action potential duration, and increased calcium transient frequency. Of the 29 candidate genes, the top five most stably ranked genes were ABL1, RPL37A, POP4, RPL30, and EIF2B1. After normalization using ABL1, KCNJ2 was significantly upregulated in the AF model; Conclusions: In the hiPSC-AMs AF model established by HS, ABL1 provides greater normalization efficiency than commonly used GAPDH.

Identifiants

pubmed: 39455925
doi: 10.1186/s12864-024-10922-x
pii: 10.1186/s12864-024-10922-x
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1001

Subventions

Organisme : Sichuan Province Science and Technology Support Program
ID : 2022YFS0610
Organisme : Sichuan Province Science and Technology Support Program
ID : 2022YFS0617
Organisme : Luzhou Science and Technology Bureau
ID : 2021LZXNYD-J26
Organisme : Luzhou Science and Technology Bureau
ID : 2021LZXNYD-Z07
Organisme : Key Laboratory of Medical Electrophysiology of Ministry of Education
ID : KeyME- 2023-01

Informations de copyright

© 2024. The Author(s).

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Auteurs

Lei Li (L)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China.
Cardiovascular Remodeling and Dysfunction Key Laboratory of Luzhou, Luzhou, China.

Zijuan Zhao (Z)

Department of Nursing, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.

Zihao Liu (Z)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China.
Cardiovascular Remodeling and Dysfunction Key Laboratory of Luzhou, Luzhou, China.

Yuquan Tang (Y)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China.

Tan Yang (T)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China.

Nailin Gong (N)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China.

Bing Liao (B)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China.
Cardiovascular Remodeling and Dysfunction Key Laboratory of Luzhou, Luzhou, China.
Metabolic Vascular Disease Key Laboratory of Sichuan Province, Luzhou, 646000, China.
Key Laboratory of Medical Electrophysiology, Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, 646000, China.

Yang Long (Y)

Metabolic Vascular Disease Key Laboratory of Sichuan Province, Luzhou, 646000, China.

Yongmei Nie (Y)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China. nieyongmei@126.com.
Cardiovascular Remodeling and Dysfunction Key Laboratory of Luzhou, Luzhou, China. nieyongmei@126.com.

Fengxu Yu (F)

Department of Cardiovascular Surgery, The Affiliated Hospital of Southwest Medical University, NO25, Taiping Street, Luzhou City, 646000, China. yuluchuan@163.com.
Cardiovascular Remodeling and Dysfunction Key Laboratory of Luzhou, Luzhou, China. yuluchuan@163.com.

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