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在新生大鼠中，miR-29a通过β1甲状腺激素受体激活α-心肌肌球蛋白重链的表达。

miR-29a activates expression of α-cardiac myosin heavy chain via β1 thyroid hormone receptor in neonatal rats.

作者信息

Wang Chengbin, He Ru, Liu Xiaohui, Li Junhua, Pan Rui

机构信息

Departments of Pediatrics, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.

出版信息

Arch Med Sci. 2020 Jan 8;20(2):641-654. doi: 10.5114/aoms.2019.91495. eCollection 2024.

DOI:10.5114/aoms.2019.91495
PMID:38757019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11094831/
Abstract

INTRODUCTION

MicroRNAs (miRs) are small noncoding RNAs which are regulators of gene expression and also regulate the genes in heart tissues. The aim of the study was to evaluate the effect of miRs on the expression level of myosin heavy chain (MHC), which is responsible for regulation of cardiac functions in neonatal rat ventricular myocytes and mice.

MATERIAL AND METHODS

The miRs were suppressed in neonatal rat ventricular myocytes using small interfering RNAs (siRNAs) against Dicer followed by evaluation of MHC levels. For study the C57 black/6 Jacksonian mice were subjected to the transverse aortic constriction (TAC) procedure.

RESULTS

The Dicer siRNA suppressed the endogenous miRs and the α-MHC gene but failed to down-regulate the β-MHC. Among the 17 selected miRs, miR-29a was found to up-regulate the α-MHC gene significantly but not β-MHC. The expression of α-MHC was suppressed by silencing the expression of miR-29a. Bioinformatics study done by TargetScan suggested thyroid hormone receptor-β1 (TR-β1) as a potential target of miR-29a. Additionally, miR-29a was found to regulate the expression of α-MHC via TR-β1 signaling.

CONCLUSIONS

The findings of the present study indicated that miR-29a modulates expression of α-the MHC gene by targeting TR-β1 in cardiac cells. The study may provide a new direction for treating cardiac failure and cardiac hypertrophy.

摘要

引言

微小RNA（miR）是一类小的非编码RNA，是基因表达的调节因子，也调节心脏组织中的基因。本研究的目的是评估miR对肌球蛋白重链（MHC）表达水平的影响，MHC负责调节新生大鼠心室肌细胞和小鼠的心脏功能。

材料与方法

使用针对Dicer的小干扰RNA（siRNA）抑制新生大鼠心室肌细胞中的miR，随后评估MHC水平。为了进行研究，对C57黑/6杰克逊小鼠进行横向主动脉缩窄（TAC）手术。

结果

Dicer siRNA抑制内源性miR和α-MHC基因，但未能下调β-MHC。在17个选定的miR中，发现miR-29a可显著上调α-MHC基因，但对β-MHC无此作用。通过沉默miR-29a的表达，α-MHC的表达受到抑制。TargetScan进行的生物信息学研究表明，甲状腺激素受体-β1（TR-β1）是miR-29a的潜在靶点。此外，发现miR-29a通过TR-β1信号通路调节α-MHC的表达。

结论

本研究结果表明，miR-29a通过靶向心脏细胞中的TR-β1调节α-MHC基因的表达。该研究可能为治疗心力衰竭和心脏肥大提供新的方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/6dbefa8eb63b/AMS-20-2-114628-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/a71b39ed6aaf/AMS-20-2-114628-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/70b17353806e/AMS-20-2-114628-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/c164c1429a8c/AMS-20-2-114628-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/a1c8d9af2f12/AMS-20-2-114628-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/ec1afb7f361b/AMS-20-2-114628-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/6dbefa8eb63b/AMS-20-2-114628-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/a71b39ed6aaf/AMS-20-2-114628-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/07955ee7380b/AMS-20-2-114628-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/0d9fadfee01f/AMS-20-2-114628-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/70b17353806e/AMS-20-2-114628-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/c164c1429a8c/AMS-20-2-114628-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/a1c8d9af2f12/AMS-20-2-114628-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/ec1afb7f361b/AMS-20-2-114628-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be6/11094831/6dbefa8eb63b/AMS-20-2-114628-g008.jpg

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