» Articles » PMID: 24728214

Global MicroRNA Profiles and Signaling Pathways in the Development of Cardiac Hypertrophy

Overview
Date 2014 Apr 15
PMID 24728214
Citations 30
Authors
Affiliations
Soon will be listed here.
Abstract

Hypertrophy is a major predictor of progressive heart disease and has an adverse prognosis. MicroRNAs (miRNAs) that accumulate during the course of cardiac hypertrophy may participate in the process. However, the nature of any interaction between a hypertrophy-specific signaling pathway and aberrant expression of miRNAs remains unclear. In this study, Spague Dawley male rats were treated with transverse aortic constriction (TAC) surgery to mimic pathological hypertrophy. Hearts were isolated from TAC and sham operated rats (n=5 for each group at 5, 10, 15, and 20 days after surgery) for miRNA microarray assay. The miRNAs dysexpressed during hypertrophy were further analyzed using a combination of bioinformatics algorithms in order to predict possible targets. Increased expression of the target genes identified in diverse signaling pathways was also analyzed. Two sets of miRNAs were identified, showing different expression patterns during hypertrophy. Bioinformatics analysis suggested the miRNAs may regulate multiple hypertrophy-specific signaling pathways by targeting the member genes and the interaction of miRNA and mRNA might form a network that leads to cardiac hypertrophy. In addition, the multifold changes in several miRNAs suggested that upregulation of rno-miR-331*, rno-miR-3596b, rno-miR-3557-5p and downregulation of rno-miR-10a, miR-221, miR-190, miR-451 could be seen as biomarkers of prognosis in clinical therapy of heart failure. This study described, for the first time, a potential mechanism of cardiac hypertrophy involving multiple signaling pathways that control up- and downregulation of miRNAs. It represents a first step in the systematic discovery of miRNA function in cardiovascular hypertrophy.

Citing Articles

MiR-451 in Inflammatory Diseases: Molecular Mechanisms, Biomarkers, and Therapeutic Applications-A Comprehensive Review Beyond Oncology.

Wang F, Mu G, Yu Z, Qin Z, Zhao X, Shi Z Curr Issues Mol Biol. 2025; 47(2).

PMID: 39996848 PMC: 11854642. DOI: 10.3390/cimb47020127.


A Thorough Navigation of miRNA's Blueprint in Crafting Cardiovascular Fate.

Nazir A, Uwishema O, Shariff S, Franco W, El Masri N, Ayele N Health Sci Rep. 2024; 7(11):e70136.

PMID: 39502130 PMC: 11535861. DOI: 10.1002/hsr2.70136.


The Epigenetic Role of MiRNAs in Endocrine Crosstalk Between the Cardiovascular System and Adipose Tissue: A Bidirectional View.

Soci U, Cavalcante B, Improta-Caria A, Roever L Front Cell Dev Biol. 2022; 10:910884.

PMID: 35859891 PMC: 9289671. DOI: 10.3389/fcell.2022.910884.


MicroRNA-34c-5p provokes isoprenaline-induced cardiac hypertrophy by modulating autophagy targeting ATG4B.

Zhang Y, Ding Y, Li M, Yuan J, Yu Y, Bi X Acta Pharm Sin B. 2022; 12(5):2374-2390.

PMID: 35646533 PMC: 9136534. DOI: 10.1016/j.apsb.2021.09.020.


MicroRNA Alterations Induced in Human Skin by Diesel Fumes, Ozone, and UV Radiation.

Valacchi G, Pambianchi E, Coco S, Pulliero A, Izzotti A J Pers Med. 2022; 12(2).

PMID: 35207665 PMC: 8880698. DOI: 10.3390/jpm12020176.


References
1.
Smits M, Mir S, Nilsson R, Van der Stoop P, Niers J, Marquez V . Down-regulation of miR-101 in endothelial cells promotes blood vessel formation through reduced repression of EZH2. PLoS One. 2011; 6(1):e16282. PMC: 3030563. DOI: 10.1371/journal.pone.0016282. View

2.
Rohini A, Agrawal N, Koyani C, Singh R . Molecular targets and regulators of cardiac hypertrophy. Pharmacol Res. 2009; 61(4):269-80. DOI: 10.1016/j.phrs.2009.11.012. View

3.
Fontana L, Sorrentino A, Condorelli G, Peschle C . Role of microRNAs in haemopoiesis, heart hypertrophy and cancer. Biochem Soc Trans. 2008; 36(Pt 6):1206-10. DOI: 10.1042/BST0361206. View

4.
Callis T, Wang D . Taking microRNAs to heart. Trends Mol Med. 2008; 14(6):254-60. DOI: 10.1016/j.molmed.2008.03.006. View

5.
Cuellar T, McManus M . MicroRNAs and endocrine biology. J Endocrinol. 2006; 187(3):327-32. DOI: 10.1677/joe.1.06426. View