15 results match your criteria mir-129-5p cardiac

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Exosomes derived from miR-129-5p modified bone marrow mesenchymal stem cells represses ventricular remolding of mice with myocardial infarction.

J Tissue Eng Regen Med 2021 Nov 23. Epub 2021 Nov 23.

Department of cardiology, Shijiazhuang People's Hospital, 5 Fangbei Road, Shijiazhuang, Hebei, 050011, China.

Background: Myocardial infraction (MI) is a severe disease with great mortality. Mesenchymal stem cells (MSCs)-derived exosomes display protection against MI. MicroRNA-129-5p was reported to exert anti-inflammation activity by targeting high mobility group box 1 (HMGB1). Read More

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November 2021

MiR-129-5p Protects H9c2 Cardiac Myoblasts From Hypoxia/Reoxygenation Injury by Targeting TRPM7 and Inhibiting NLRP3 Inflammasome Activation.

J Cardiovasc Pharmacol 2021 05;77(5):586-593

Department of Cardiology, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China.

Abstract: As a biomarker for heart failure, miR-129-5p is abnormally expressed during myocardial I/R, but its specific functions and mechanisms remain largely unclear. Thus, this study explored the roles and possible mechanisms of miR-129-5p in hypoxia/reoxygenation (H/R)-insulted H9c2 cardiac myoblasts. After H/R insult, miR-129-5p expression levels were decreased, along with reduced cell viability and enhanced lactate dehydrogenase release in H9c2 cells. Read More

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Clinical significance of the long non-coding RNA NEAT1/miR-129-5p axis in the diagnosis and prognosis for patients with chronic heart failure.

Exp Ther Med 2021 May 19;21(5):512. Epub 2021 Mar 19.

Department of Anesthesiology, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China.

Chronic heart failure (CHF) is the leading cause of death worldwide. The regulatory interactions of long non-coding RNA (lncRNAs) and microRNAs (miRs) have important roles in multiple diseases. However, the clinical significance of the nuclear-enriched abundant transcript 1 (NEAT1)/miR-129-5p axis in CHF has remained elusive. Read More

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The protective effects of the miR-129-5p/keap-1/Nrf2 axis on Ang II-induced cardiomyocyte hypertrophy.

Ann Transl Med 2021 Jan;9(2):154

Department of Cardiology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.

Background: Cardiac hypertrophy is a common pathological process in many cardiac diseases, and persistent cardiac hypertrophy is the main cause of heart failure and sudden cardiogenic death. Thus, it is essential to elucidate the mechanism of cardiac hypertrophy to ensure better prevention and treatment.

Methods: The Human cardiac myocytes (HCMs) were incubated with 100 nmol/L Ang II (Sigma) for 48 hours to induce the in vitro cardiomyocyte hypertrophy model. Read More

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January 2021

miR-129-5p ameliorates ischemia-reperfusion injury by targeting HMGB1 in myocardium.

Gen Physiol Biophys 2020 Sep;39(5):461-470

Second Department of Cardiovascular Medicine, Cangzhou Central Hospital, Cangzhou, Hebei, People's Republic of China.

Globally, acute myocardial infarction (AMI) is a serious condition affecting millions of individuals. While AMI therapy improves blood flow during surgery, reperfusion-induced injury may also occur, leading to secondary cardiac damage or even death. Here, we investigated miR-129-5p in myocardial ischemia-reperfusion (I/R) injury in rats, to explore reperfusion-related molecular mechanisms in myocardium. Read More

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September 2020

Promoting role of circ-Jarid2/miR-129-5p/Celf1 axis in cardiac hypertrophy.

Gene Ther 2020 Jul 6. Epub 2020 Jul 6.

Department of Cardiology, Jiangxi Provincial People's Hospital Affiliated to Nanchang University, Nanchang, 330006, Jiangxi, China.

Cardiac hypertrophy is imposed much pressure on heart and threatening our live. Previous study suggested that dysregulation of Celf1 is largely connecting to neonatal cardiac dysfunction. Hence, we aimed to explore the precise function and probable regulatory mechanism upstream of Celf1in cardiac hypertrophy. Read More

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MiR-129-5p protects against myocardial ischemia-reperfusion injury via targeting HMGB1.

Eur Rev Med Pharmacol Sci 2020 04;24(8):4440-4450

Department of Laboratory Medicine, Houjie Hospital of Dongguan, Dongguan, P.R. China.

Objective: To investigate the protective effect of miR-129-5p on ischemia-reperfusion (I/R) injury via targeting high mobility group box-1 (HMGB1).

Materials And Methods: Rat models of myocardial I/R and hypoxia/reoxygenation (H/R) cardiomyocytes were established, and the miR-129-5p and HMGB1 expression levels in myocardium of I/R rats and in cardiomyocytes of H/R rats were quantified by RT-PCR. The over-expression of miR-129-5p was performed on I/R rats, and the over-expression of miR-129-5p and down-regulation of HMGB1 were performed on cardiomyocytes of H/R rats. Read More

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miR-129-5p attenuates hypoxia-induced apoptosis in rat H9c2 cardiomyocytes by activating autophagy.

J Gene Med 2020 08 29;22(8):e3200. Epub 2020 Apr 29.

Department of Geriatric Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Background: Autophagy is closely associated with apoptosis in H9c2 cardiomyocytes as a result of hypoxia. The present study aimed to determine whether microRNAs (miRs) mediated apoptosis and autophagy in hypoxia-stimulated H9c2 cardiomyocytes.

Methods: miR microarrays and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assays were used to detect differentially expressed miRs in H9c2 cardiomyocytes following hypoxia stimulation. Read More

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MiR-129-5p alleviates myocardial injury by targeting suppressor of cytokine signaling 2 after ischemia/reperfusion.

Kaohsiung J Med Sci 2020 Aug 7;36(8):599-606. Epub 2020 Apr 7.

Department of Cardiology, Wuhan Third Hospital-Tongren Hospital of Wuhan University, Wuhan, China.

Acute myocardial infarction (AMI) remains one of the leading causes of morbidity and mortality worldwide. Ischemia/reperfusion (I/R), the most common consequence of AMI treatment, may induce severe myocardial cell injury, yet the precise mechanism continues to be enigmatic. In the present study, we found that miR-129-5p was significantly downregulated in mouse I/R model. Read More

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Long Noncoding RNA NEAT1 Promotes Myocardiocyte Apoptosis and Suppresses Proliferation Through Regulation of miR-129-5p.

J Cardiovasc Pharmacol 2019 12;74(6):535-541

Department of Cardiology, The First Hospital of Jilin University, Changchun City, Jilin Province, P.R. China.

Recent studies have revealed the important role of long noncoding RNAs (lncRNAs) in heart development and pathogenesis. This study was aimed to investigate the role of NEAT1 in hypoxia-induced cardiac injury and explore its possible molecular mechanism. Real-time PCR (RT-PCR) was used to determine the relative RNA expression of NEAT1 and its potential target microRNA, miR-129-5p, in the plasma of patients with acute myocardial infarction, heart failure, and angina, as well as in H2O2-treated H9c2 cells. Read More

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December 2019

miR-129-5p improves cardiac function in rats with chronic heart failure through targeting HMGB1.

Mamm Genome 2019 10 23;30(9-10):276-288. Epub 2019 Oct 23.

Department Cardiovascular V, Cangzhou Central Hospital, No. 16 Xinhua West Road, Cangzhou, 061000, Hebei, China.

Increasing evidence shows that miRNAs play pivotal roles in cardiovascular diseases, including heart failure (HF). The aim of this study was to investigate the role of miR-129-5p in chronic heart failure and the underlying mechanisms. The levels of miR-129-5p and HMGB1 in chronic heart failure patients (CHF) and normal controls were examined by RT-qPCR and ELISA. Read More

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October 2019

MiR-129-5p inhibits autophagy and apoptosis of H9c2 cells induced by hydrogen peroxide via the PI3K/AKT/mTOR signaling pathway by targeting ATG14.

Biochem Biophys Res Commun 2018 11 19;506(1):272-277. Epub 2018 Oct 19.

Department of Cardiology, Cangzhou Central Hospital, Hebei, 061001, PR China. Electronic address:

Ischemic heart disease (IHD) is a significant cause of cardiovascular diseases. MicroRNAs (miRNAs) have been thought to be critical regulators in the heart diseases. The present study was aimed to investigate the effect of miR-129-5p on the autophagy and apoptosis by targeting ATG14 as well as how miR-129-5p worked through the PI3K/AKT/mTOR signaling pathway in HO-induced H9c2 cells. Read More

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November 2018

Microarray-based bioinformatics analysis of the combined effects of SiNPs and PbAc on cardiovascular system in zebrafish.

Chemosphere 2017 Oct 28;184:1298-1309. Epub 2017 Jun 28.

Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, PR China; Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing 100069, PR China.

With rapid development of nanotechnology and growing environmental pollution, the combined toxic effects of SiNPs and pollutants of heavy metals like lead have received global attentions. The aim of this study was to explore the cardiovascular effects of the co-exposure of SiNPs and lead acetate (PbAc) in zebrafish using microarray and bioinformatics analysis. Although there was no other obvious cardiovascular malformation except bleeding phenotype, bradycardia, angiogenesis inhibition and declined cardiac output in zebrafish co-exposed of SiNPs and PbAc at NOAEL level, significant changes were observed in mRNA and microRNA (miRNA) expression patterns. Read More

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October 2017

A microRNA-129-5p/Rbfox crosstalk coordinates homeostatic downscaling of excitatory synapses.

EMBO J 2017 06 9;36(12):1770-1787. Epub 2017 May 9.

Biochemisch-Pharmakologisches Centrum, Institut für Physiologische Chemie, Philipps-Universität Marburg, Marburg, Germany

Synaptic downscaling is a homeostatic mechanism that allows neurons to reduce firing rates during chronically elevated network activity. Although synaptic downscaling is important in neural circuit development and epilepsy, the underlying mechanisms are poorly described. We performed small RNA profiling in picrotoxin (PTX)-treated hippocampal neurons, a model of synaptic downscaling. Read More

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Trichostatin A induces a unique set of microRNAs including miR-129-5p that blocks cyclin-dependent kinase 6 expression and proliferation in H9c2 cardiac myocytes.

Mol Cell Biochem 2016 Apr 5;415(1-2):39-49. Epub 2016 Mar 5.

Department of Veterans Affairs Medical Center, Memphis, TN, 38104, USA.

The pan-histone deacetylase inhibitor (HDACI), trichostatin A (TSA), was shown to normalize interleukin-18-induced cardiac hypertrophy in vivo and in vitro; evidently, this occurred via epigenetic mechanisms that profoundly altered cardiac gene expression (Majumdar et al. in, Physiol Genom, 43: 1392, 2011; BMC Genom, 13: 709, 2012). Here, we tested the hypothesis that TSA-induced changes in chromatin architecture also led to altered expression of microRNAs that in turn, contributed to the unique transcriptome of cardiac myocytes exposed to the HDACI. Read More

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