MicroRNA‑133b alleviates doxorubicin‑induced cardiomyocyte apoptosis and cardiac fibrosis by targeting PTBP1 and TAGLN2

Li, Zhen; Ye, Zekang; Ma, Jiazheng; Gu, Qian; Teng, Jianzhen; Gong, Xiaoxuan

doi:10.3892/ijmm.2021.4958

Cited by 19 publications

(15 citation statements)

References 46 publications

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“…Previous studies have reported that RHD (Rh blood group D antigen) [154], S100A12 [155], TXN (thioredoxin) [156], TLR9 [157], S100P [158], TAGLN2 [159], S100A9 [160], CA1 [161], HP (haptoglobin) [162], RPL39 [163], F5 [164], PINK1 [165], B2M [166], S100A11 [167], SLC4A1 [168], CBS (cystathionine beta-synthase) [169], AHSP (alpha hemoglobin stabilizing protein) [170], F12 [171], EPHB4 [172], NFE2 [173], VRK1 [174], GPX1 [175], FOXA1 [176], CYP11B2 [177], NOX1 [178], IL33 [179], NPHS1 [180], OTC (ornithine transcarbamylase) [181], SULF1 [182], CYP1A1 [183], DCN (decorin) [184], ADAMTS7 [185], WNT4 [186], LAMA4 [187], SCN4A [188], CACNB2 [189], GNB3 [190], ENPEP (glutamyl aminopeptidase) [191], WNK4 [192], FOXC1 [193], PAX8 [194], ROBO1 [195], CXCL8 [196], PAPPA2 [197], LOX (lysyl oxidase) [198], NOSTRIN (nitric oxide synthase trafficking) [199], MUC16 [200], MIOX (myo-inositol oxygenase) [201], CYP11A1 [202] and CYP3A5 [203] are involved in the pregnancy complications. Modification in the activity and expression of RHD (Rh blood group D antigen) [204], S100A12 [205], TLR9 [206], ANXA3 [207], S100P [208], TAGLN2 [209], S100A9 [210], KCNH2 [211], HP (haptoglobin) [212], SELENBP1 [213], TANGO2 [214], PINK1 [215], TFR2 [216], B2M [217], LTBP2 [218], PGLYRP1 [219], HRH2 [220], CLEC5A [221], PLSCR4 [222], S100A11 [223], PPBP (pro-platelet basic protein) [224], RAP1GAP […”

Section: Discussionmentioning

confidence: 99%

Identification of Key Genes and Biological Pathways in Bipolar Disorder by Bioinformatics and Next Generation Sequencing Data Analysis

Vastrad¹,

Vastrad²

2022

Preprint

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Bipolar disorder (BD), also known as psychiatric disorder, affects millions of people all over the world. The aim of this investigation was to screen and verify hub genes involved in BD as well as to explore potential molecular mechanisms. The next generation sequencing (NGS) dataset GSE124326 was downloaded from the Gene Expression Omnibus (GEO) database, which contained 480 samples, including 240 BD and 240 normal controls. Differentially expressed genes (DEGs) were filtered and subjected to gene ontology (GO) and pathway enrichment analyses. A protein–protein interaction (PPI) network and module analysis were used to identify hub genes. The miRNA-hub gene regulatory network and TF-hub gene regulatory network were also constructed. Receiver operating characteristic curve (ROC) analysis was used to validate hub genes. In this work, 957 DEGs, including 477 up regulated and 480 down regulated, were obtained from NGS data. The GO and pathway enrichment analyses of the DEGs showed that the up regulated genes were enriched in the neutrophil degranulation, immune system, transport, cytoplasm and enzyme regulator activity, and the down regulated genes were enriched in extracellular matrix organization, diseases of metabolism, multicellular organismal process, cell periphery and metal ion binding. Finally, through analyzing the PPI network, miRNA-hub gene regulatory network and TF-hub gene regulatory network, we screened hub genes UBB, UBE2D1, TUBA1A, RPL11, RPS24, NOTCH3, CAV1, CNBD2, CCNA1 and MYH11 by the Cytoscape software. The current investigation illustrates a characteristic NGS data in BD, which might contribute to the interpretation of the progression of BD and provide novel biomarkers and therapeutic targets for BD.

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Section: Discussionmentioning

confidence: 99%

Identification of Key Genes and Biological Pathways in Bipolar Disorder by Bioinformatics and Next Generation Sequencing Data Analysis

Vastrad¹,

Vastrad²

2022

Preprint

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“…In addition, the previous study has shown that miR-140-5p could aggravate DOX-induced cardiotoxicity via targeting both Nrf2 and Sirt2 [ 17 ]. Plenty of evidences have shown that miRNAs are engaged in DOX-induced cardiotoxicity, such miR-133b [ 19 ], miR-98 [ 20 ] and miR-152 [ 21 ]. However, it is still unclear whether miR-140-5p is involved in limonin-mediated protection on DOX-induced cardiotoxicity, which could be explored in the future.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of limonin against doxorubicin-induced cardiotoxicity via activating nuclear factor - like 2 and Sirtuin 2 signaling pathways

Deng

Huang

2021

Bioengineered

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The anti-tumor and anti-inflammatory effects of limonin have been established, here, we aim to explore whether limonin can induce protective effects against doxorubicin (DOX)-mediated cardiotoxicity which limits its clinical application. We found that limonin attenuated DOX-mediated cytoxicology of myocardial cell line H9C2 by measuring cell viability and reactive oxygen species (ROS) level.Additionally, limonin ameliorates DOX-induced cardiac injury in rat by examining the activity of lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) R I P T concentration, and histopathological changes. Mechanistically, it was shown that limonin partially abrogated the inhibition of Nuclear factor -like 2 and Sirtuin 2 signaling induced by DOX. Furthermore, limonin-mediated protective effects on DOX-mediated cytoxicology of H9C2 were rescued by a Sirt2-specific inhibitor or siRNA against Sirt2. Thus, this work reveals that limonin can suppress DOX-mediated cardiotoxicity through activating Nrf2 and Sirt2 signaling.

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“…PTB1 and TGLN2 serve as downstream targets of miR-133b. Overexpression of PTBP1 or TAGLN2 reversed the protective effects of miR-133 [ 293 ], indicating that miR-133 protects against DOX-induced apoptosis and cardiac fibrosis by inhibiting the expression of PTB1 and TAGLN2. Therefore, miR-133 may serve as a potential biomarker in the diagnosis and treatment of DOX-induced cardiotoxicity, leading to the development of DCM.…”

Section: Ncrnasmentioning

confidence: 99%

Long non-coding RNAs and microRNAs as crucial regulators in cardio-oncology

et al. 2022

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Cancer is one of the leading causes of morbidity and mortality worldwide. Significant improvements in the modern era of anticancer therapeutic strategies have increased the survival rate of cancer patients. Unfortunately, cancer survivors have an increased risk of cardiovascular diseases, which is believed to result from anticancer therapies. The emergence of cardiovascular diseases among cancer survivors has served as the basis for establishing a novel field termed cardio-oncology. Cardio-oncology primarily focuses on investigating the underlying molecular mechanisms by which anticancer treatments lead to cardiovascular dysfunction and the development of novel cardioprotective strategies to counteract cardiotoxic effects of cancer therapies. Advances in genome biology have revealed that most of the genome is transcribed into non-coding RNAs (ncRNAs), which are recognized as being instrumental in cancer, cardiovascular health, and disease. Emerging studies have demonstrated that alterations of these ncRNAs have pathophysiological roles in multiple diseases in humans. As it relates to cardio-oncology, though, there is limited knowledge of the role of ncRNAs. In the present review, we summarize the up-to-date knowledge regarding the roles of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in cancer therapy-induced cardiotoxicities. Moreover, we also discuss prospective therapeutic strategies and the translational relevance of these ncRNAs.

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MicroRNA‑133b alleviates doxorubicin‑induced cardiomyocyte apoptosis and cardiac fibrosis by targeting PTBP1 and TAGLN2

Cited by 19 publications

References 46 publications

Identification of Key Genes and Biological Pathways in Bipolar Disorder by Bioinformatics and Next Generation Sequencing Data Analysis

Identification of Key Genes and Biological Pathways in Bipolar Disorder by Bioinformatics and Next Generation Sequencing Data Analysis

Protective effect of limonin against doxorubicin-induced cardiotoxicity via activating nuclear factor - like 2 and Sirtuin 2 signaling pathways

Long non-coding RNAs and microRNAs as crucial regulators in cardio-oncology

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