Publications by authors named "Rubing Wu"

3 Publications

  • Page 1 of 1

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). In the present study, the effects of MSCs-derived exosomes overexpressing miR-129-5p on MI were evaluated.

Methods: Bone marrow mesenchymal stem cells (BMSCs) were transfected with miR-129-5p for exosomes isolation. MI mice model was established and administrated exosomes overexpressing miR-129-5p. The cardiac function, expression of HMGB1,inflammatory cytokines, apoptosis and fibrosis in heart tissues were measured.

Resutls: MiR-129-5p inhibited HMGB1 expression in BMSCs. MI mice treated with exosomes overexpressing miR-129-5p had enhanced cardiac function and decreased expression of HMGB1 and production of inflammatory cytokines. Exosomes overexpressing miR-129-5p further prevented apoptosis and fibrosis.

Conclusion: Exosome-mediated transfer of miR-129-5p suppressed inflammation in MI mice by targeting HMGB1. This article is protected by copyright. All rights reserved.
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November 2021

Uncovering Potential lncRNAs and mRNAs in the Progression From Acute Myocardial Infarction to Myocardial Fibrosis to Heart Failure.

Front Cardiovasc Med 2021 16;8:664044. Epub 2021 Jul 16.

Department of Cardiovasology, Shijiazhuang People's Hospital, Shijiazhuang, China.

Morbidity and mortality of heart failure (HF) post-myocardial infarction (MI) remain elevated. The aim of this study was to find potential long non-coding RNAs (lncRNAs) and mRNAs in the progression from acute myocardial infarction (AMI) to myocardial fibrosis (MF) to HF. Firstly, blood samples from AMI, MF, and HF patients were used for RNA sequencing. Secondly, differentially expressed lncRNAs and mRNAs were obtained in MF vs. AMI and HF vs. MF, followed by functional analysis of shared differentially expressed mRNAs between two groups. Thirdly, interaction networks of lncRNA-nearby targeted mRNA and lncRNA-co-expressed mRNA were constructed in MF vs. AMI and HF vs. MF. Finally, expression validation and diagnostic capability analysis of selected lncRNAs and mRNAs were performed. Several lncRNA-co-expressed/nearby targeted mRNA pairs including AC005392.3/AC007278.2-IL18R1, AL356356.1/AL137145.2-PFKFB3, and MKNK1-AS1/LINC01127-IL1R2 were identified. Several signaling pathways including TNF and cytokine-cytokine receptor interaction, fructose and mannose metabolism and HIF-1, hematopoietic cell lineage and fluid shear stress, and atherosclerosis and estrogen were selected. IL1R2, IRAK3, LRG1, and PLAC4 had a potential diagnostic value for both AMI and HF. Identified AC005392.3/AC007278.2-IL18R1, AL356356.1/AL137145.2-PFKFB3, and MKNK1-AS1/LINC01127-IL1R2 lncRNA-co-expressed/nearby targeted mRNA pairs may play crucial roles in the development of AMI, MF, and HF.
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July 2021

Effects of Atrial Fibrillation-Derived Exosome Delivery of miR-107 to Human Umbilical Vein Endothelial Cells.

DNA Cell Biol 2021 Apr 2;40(4):568-579. Epub 2021 Mar 2.

Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

The aim of this study was to explore the effects of atrial fibrillation (AF)-derived exosome delivery of miR-107 to human umbilical vein endothelial cells (HUVECs) and its related mechanisms. Exosomes were isolated from the plasma of patients with AF and healthy controls, followed by characterization. The expression levels of miR-320d, miR-103a-3p, and miR-107 were measured using real-time quantitative PCR (RT-qPCR). The dual-luciferase reporter gene was used to verify the downstream target of miR-107. Afterward, HUVECs were treated with AF-derived exosomes or transfected with miR-107 mimics. After cell culture, Cell Counting Kit-8, Transwell, and flow cytometry were used to determine cell viability, migration, and apoptosis and cell cycle phase. Finally, RT-qPCR was performed to examine the expression of related genes. NanoSight, transmission electron microscopy, and western blotting showed that exosomes were successfully isolated, and that AF-derived exosomes could be taken up by HUVECs. The expression of miR-107 was significantly higher in AF-derived exosomes than in normal exosomes ( < 0.05). was shown to be the direct target of miR-107. In addition, miR-107 mimics and AF-derived exosomes significantly suppressed cell viability and migration ( < 0.05) and enhanced cell apoptosis; they also increased G0/G1-phase cells and reduced S-phase cells. RT-qPCR showed that exosomal miR-107 overexpression significantly downregulated the expression of and ( < 0.05), whereas it markedly upregulated the expression of , and ( < 0.05). AF-derived exosomes can deliver miR-107 to HUVECs, and exosomal miR-107 may regulate cell viability, migration, and apoptosis and cell cycle progression by mediating the miR-107/USP14 pathway.
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April 2021