Involvement of microRNA-23b-5p in the promotion of cardiac hypertrophy and dysfunction via the HMGB2 signaling pathway

Oumarou, Diafara Boureima; Ji, Heyu; Xu, Junmei; Li, Suobei; Ruan, Wei; Xiao, Feng; Yu, Fei

doi:10.1016/j.biopha.2019.108977

Cited by 26 publications

(16 citation statements)

References 21 publications

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“…A gain-of function study revealed that the hypertrophic effects of miR-23b-5p overexpression observed in the Ang-II- and TAC-induced cardiac hypertrophy models was mediated via targeting high-mobility group box 2 (HMGB2) [97], a nuclear protein that regulates gene transcription, DNA recombination and repair, cell replication, and autophagy [98].…”

Section: Micrornas That Promote Cardiac Hypertrophymentioning

confidence: 99%

MicroRNAs in Cardiac Hypertrophy

Wehbe

Nasser

Pintus

et al. 2019

IJMS

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Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy.

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Section: Micrornas That Promote Cardiac Hypertrophymentioning

confidence: 99%

MicroRNAs in Cardiac Hypertrophy

Wehbe

Nasser

Pintus

et al. 2019

IJMS

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“…Imbalanced microRNA expression in the progenitor cells of the developing heart might cause congenital and/or structural defects, including altered cell migration and proliferation, as well as inappropriate cell type specification (Pang et al, 2019;Kalayinia et al, 2021). In particular, it has been reported that: 1) miR-23b is upregulated in cardiac hypertrophy, and its overexpression in cardiomyocytes in vitro is sufficient to promote hypertrophic growth (Thum et al, 2008;Boureima Oumarou et al, 2019); 2) miR-130a is required for adequate proliferation of cardiac progenitors (Kim et al, 2009), supported by gain-offunction murine experiments, leading to cardiomyocyte proliferation defects as ventricular hypoplasia; 3) miR-106a is significantly upregulated in cardiac hypertrophy, as demonstrated by in vivo and in vitro analyses (Guan et al, 2016); and 4) although miR-100 function is not relevant to hypertrophic gene expression, its role in cardiac regeneration has been widely demonstrated in zebrafish and mice, and it also plays specific roles in adult isoform cardiac gene regulation (Tarantino et al, 2010;Aguirre et al, 2014). Since these microRNAs have proved significant in cardiac structural and functional features, we will proceed to discuss their relevance during cardiac development.…”

Section: Discussionmentioning

confidence: 99%

Dynamic MicroRNA Expression Profiles During Embryonic Development Provide Novel Insights Into Cardiac Sinus Venosus/Inflow Tract Differentiation

García-Padilla

Dueñas

Franco

et al. 2022

Front. Cell Dev. Biol.

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MicroRNAs have been explored in different organisms and are involved as molecular switches modulating cellular specification and differentiation during the embryonic development, including the cardiovascular system. In this study, we analyze the expression profiles of different microRNAs during early cardiac development. By using whole mount in situ hybridization in developing chick embryos, with microRNA-specific LNA probes, we carried out a detailed study of miR-23b, miR-130a, miR-106a, and miR-100 expression during early stages of embryogenesis (HH3 to HH17). We also correlated those findings with putative microRNA target genes by means of mirWalk and TargetScan analyses. Our results demonstrate a dynamic expression pattern in cardiac precursor cells from the primitive streak to the cardiac looping stages for miR-23b, miR-130a, and miR-106a. Additionally, miR-100 is later detectable during cardiac looping stages (HH15-17). Interestingly, the sinus venosus/inflow tract was shown to be the most representative cardiac area for the convergent expression of the four microRNAs. Through in silico analysis we revealed that distinct Hox family members are predicted to be targeted by the above microRNAs. We also identified expression of several Hox genes in the sinus venosus at stages HH11 and HH15. In addition, by means of gain-of-function experiments both in cardiomyoblasts and sinus venosus explants, we demonstrated the modulation of the different Hox clusters, Hoxa, Hoxb, Hoxc, and Hoxd genes, by these microRNAs. Furthermore, we correlated the negative modulation of several Hox genes, such as Hoxa3, Hoxa4, Hoxa5, Hoxc6, or Hoxd4. Finally, we demonstrated through a dual luciferase assay that Hoxa1 is targeted by miR-130a and Hoxa4 is targeted by both miR-23b and miR-106a, supporting a possible role of these microRNAs in Hox gene modulation during differentiation and compartmentalization of the posterior structures of the developing venous pole of the heart.

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“…In this study, we constructed a miR-1929-3p overexpression vector coated with rAAV, which is considered as an ideal carrier for gene therapy because of low immunogenicity, nonpathogenicity, long-term expression, and serotype-dependent tissue affinity [ 33 ]. Boureima et al found that type 9 rAAV can steadily infect the myocardium of C57BL/6 mice [ 34 ]. In this study, miR-1929-3p overexpression applied at the age of 13 months (when distinct myocardial remodeling was revealed).…”

Section: Discussionmentioning

confidence: 99%

miR‐1929‐3p Overexpression Alleviates Murine Cytomegalovirus‐Induced Hypertensive Myocardial Remodeling by Suppressing Ednra/NLRP3 Inflammasome Activation

Wang

Huang

Zhong

et al. 2020

BioMed Research International

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MicroRNAs (miRNAs) play crucial roles in the development of essential hypertension (EH). Previously, we found that the expression of miR-1929-3p was decreased in C57BL/6 mice with hypertension induced by murine cytomegalovirus (MCMV). In this study, we explored the role of miR-1929-3p in hypertension myocardial remodeling in MCMV-infected mice. First, we measured MCMV DNA and host IgG and IgM after infection and determined the expression of miR-1929-3p and its target gene endothelin A receptor (Ednra) mRNA in the myocardium of mice. Then, we performed invasive blood pressure (BP) monitoring. Heart-to-body weight ratio (HW/BW%), along with mRNA levels of B-type natriuretic peptide (BNP) and beta myosin heavy chain (β-MHC), revealed myocardial remodeling. Hematoxylin/eosin and Masson’s trichrome staining indicated morphological changes in the myocardium. Cardiac function was assessed via echocardiography. Moreover, MCMV-infected mice were injected with recombinant adeno-associated virus- (rAAV-) miR-1929-3p overexpression vector. Immunohistochemistry and western blotting showed the expression of Ednra and the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. And enzyme-linked immunosorbent assay (ELISA) revealed the concentrations of endothelin-1 (ET-1), interleukin-1β (IL-1β), and interleukin-18 (IL-18). In this study, we found that decreased expression of miR-1929-3p in MCMV-infected mice induced high BP and further development of myocardial remodeling cardiac function injury through increased expression of Ednra. Strikingly, overexpression of miR-1929-3p ameliorated these pathological changes of the heart. The positive effect was shown to be associated with inhibition of NLRP3 inflammasome activation and decreased expression of key proinflammatory cytokine IL-1β. Collectively, these results indicate that miR-1929-3p overexpression may effectively alleviate EH myocardial remodeling by suppressing Ednra/NLRP3 inflammasome activation in MCMV-infected mice.

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Involvement of microRNA-23b-5p in the promotion of cardiac hypertrophy and dysfunction via the HMGB2 signaling pathway

Cited by 26 publications

References 21 publications

MicroRNAs in Cardiac Hypertrophy

MicroRNAs in Cardiac Hypertrophy

Dynamic MicroRNA Expression Profiles During Embryonic Development Provide Novel Insights Into Cardiac Sinus Venosus/Inflow Tract Differentiation

miR‐1929‐3p Overexpression Alleviates Murine Cytomegalovirus‐Induced Hypertensive Myocardial Remodeling by Suppressing Ednra/NLRP3 Inflammasome Activation

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