Academic Journal

MicroRNA‐574 regulates FAM210A expression and influences pathological cardiac remodeling

التفاصيل البيبلوغرافية
العنوان: MicroRNA‐574 regulates FAM210A expression and influences pathological cardiac remodeling
المؤلفون: Jiangbin Wu, Kadiam C Venkata Subbaiah, Feng Jiang, Omar Hedaya, Amy Mohan, Tingting Yang, Kevin Welle, Sina Ghaemmaghami, Wai Hong Wilson Tang, Eric Small, Chen Yan, Peng Yao
المصدر: EMBO Molecular Medicine, Vol 13, Iss 2, Pp 1-20 (2020)
بيانات النشر: Springer Nature, 2020.
سنة النشر: 2020
المجموعة: LCC:Medicine (General)
LCC:Genetics
مصطلحات موضوعية: cardiac remodeling, FAM210A, gene regulation, microRNA, mitochondria, Medicine (General), R5-920, Genetics, QH426-470
الوصف: Abstract Aberrant expression of mitochondrial proteins impairs cardiac function and causes heart disease. The mechanism of regulation of mitochondria encoded protein expression during cardiac disease, however, remains underexplored. Here, we show that multiple pathogenic cardiac stressors induce the expression of miR‐574 guide and passenger strands (miR‐574‐5p/3p) in both humans and mice. miR‐574 knockout mice exhibit severe cardiac disorder under different pathogenic cardiac stresses while miR‐574‐5p/3p mimics that are delivered systematically using nanoparticles reduce cardiac pathogenesis under disease insults. Transcriptomic analysis of miR‐574‐null hearts uncovers family with sequence similarity 210 member A (FAM210A) as a common target mRNA of miR‐574‐5p and miR‐574‐3p. The interactome capture analysis suggests that FAM210A interacts with mitochondrial translation elongation factor EF‐Tu. Manipulating miR‐574‐5p/3p or FAM210A expression changes the protein expression of mitochondrial‐encoded electron transport chain (ETC) genes but not nuclear‐encoded mitochondrial ETC genes in both human AC16 cardiomyocyte cells and miR‐574‐null murine hearts. Together, we discovered that miR‐574 regulates FAM210A expression and modulates mitochondrial‐encoded protein expression, which may influence cardiac remodeling in heart failure.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1757-4676
1757-4684
Relation: https://doaj.org/toc/1757-4676; https://doaj.org/toc/1757-4684
DOI: 10.15252/emmm.202012710
URL الوصول: https://doaj.org/article/4538a4478f1142fd93fb22b37a9c6ce5
رقم الانضمام: edsdoj.4538a4478f1142fd93fb22b37a9c6ce5
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:17574676
17574684
DOI:10.15252/emmm.202012710