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Adipose tissue mediate insulin resistance in obesity mice through the exosomal transfer of miR-141-3p into hepatocytes

ABSTRACT: Adipose tissue mediate insulin resistance in obesity mice through the exosomal transfer of miR-141-3p into hepatocytes

PROVIDER: PRJNA431813 | ENA |

REPOSITORIES: ENA

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Adipose tissue mediate insulin resistance in obesity mice through the exosomal transfer of miR-141-3p into hepatocytes

Project description:Exosomes which are nano-vesicles and released from living cells, have attracted more attention as an important mediator for cell-to-cell communication. Given that obesity often causes insulin resistance, it is significant to test whether exosomes derived from obesity adipose tissue possess any capacity in regulating insulin sensitivity. In this study we purified exosomes from the adipose tissue. Exosomes derived from ob/ob mice (Ob-exosomes) and B6 mice fed a high-fat diet (HFD-exosomes) displayed similar size and molecular maker to those originated from the normal B6 mice (WT-exosomes), but their regulatory role in insulin sensitivity was opposite. Abundant exosomal miRNAs were detected by the Next Generation Sequencing. Ob-exosomes encapsulated the lower levels of miR-141-3p compared to WT-exosomes, furthermore, miR-141-3p can be effectively delivered into AML12 cells accompanied by the absorption of Ob-exosomes and WT-exosomes. But the absorption of miR-141-3p from adipose tissues to AML12 cells could be blocked by GW4869, an inhibitor of exosome biogenesis and release. Importantly, the exosomal miR-141-3p functionally down-regulated its target gene Pten expression in AML12 cells, and the knockdown of miR-141-3p inhibited the insulin response and glucose uptake in AML12 cells, however Ob-exosomes-mediated inhibitory effects on insulin function disappeared after overexpression of miR-141-3p. These data indicate that the absorption of exosomes released from obesity adipose tissue including lower level of miR-141-3p than healthy adipose tissue into hepatocytes can significantly inhibit the insulin sensitivity and glucose uptake. Thus, our study may certify a novel mechanism that the secretion of “harmful” exosomes from obesity adipose tissues cause insulin resistance.

2020-01-27 | GSE109739 | GEO

Exosomal transfer of obesity adipose tissue for decreased miR-141-3p mediate insulin resistance of hepatocytes.

Project description: Not available

| S-EPMC6367552 | biostudies-literature

Exosomal hsa-miR199a-3p promotes proliferation and metastasis in neuroblastoma

Project description:To elucidate whether exosomal hsa-miR199a-3p plays a role in neuroblastoma tumorigenesis, a miRNA-seq analysis on plasma exosomal miRNA from neuroblastoma patients and normal controls.

2019-03-08 | GSE128004 | GEO

miR-141-3p regulates the expression of corneal epithelial differentiation

Project description:Corneal epithelial RCE1(5T5) cells follow a sequential process that leads to the formation of a 4-5 layered stratified epithelium with a gene expression pattern similar to that shown in primary cultures of corneal epithelial cells. We have previously identified three different developmental stages during the differentiation of the rabbit corneal epithelial cell line RCE1(5T5). In this analysis we describe the participation of miR-141-3p as a regulator of the proliferative phenotype and its participation on maintaining differentiation of corneal eptihelial cells.

2024-04-20 | GSE264014 | GEO

Effect of salivary exosomal miR-25-3p on periodontitis with insulin resistance

Project description:Effect of salivary exosomal miR-25-3p on periodontitis with insulin resistance

| PRJNA781584 | ENA

Exosomal miR-92a-3p as a diagnostic biomarker for adenomyosis and its pathological mechanism

Project description:This study aimed to elucidate the role of microRNA miR-92a-3p in the pathogenesis of adenomyosis. We focused on understanding how miR-92a-3p in exosomes derived from ectopic lesions influences the behavior of endometrial cells, DRG neurons, and Human Umbilical Vein Endothelial Cells (HUVECs), and its potential as a non-invasive diagnostic biomarker. Our findings revealed that MiR-92a-3p is significantly upregulated in exosomes derived from ectopic lesions of adenomyosis. This upregulation was associated with enhanced migration and invasion capabilities in eutopic endometrial cells, DRG neurons, and HUVECs. Furthermore, the study demonstrated a significant correlation between the levels of MiR-92a-3p in urinary exosomes and the clinical symptoms of adenomyosis, suggesting its potential as a non-invasive biomarker for the disease. This study elucidates an exosomal signaling process via miR-92a-3p that drives pathological infiltration and angiogenesis to promote adenomyosis progression. Upregulated miR-92a-3p in biofluid exosomes shows promising non-invasive biomarker potential for diagnosis and monitoring of this disease. Our findings unveil novel targets and tools for improved clinical management.

2024-04-01 | GSE262302 | GEO

Exosomal hsa-miR199a-3p promotes proliferation and metastasis in neuroblastoma

Project description:Exosomal hsa-miR199a-3p promotes proliferation and metastasis in neuroblastoma

| PRJNA526037 | ENA

Effect of salivary exosomal miR-25-3p on periodontitis with insulin resistance

Project description:Salivary exsomal miRNAs may play important role in the pathogenesis of chronic inflammatory disease, such as periodontitis. There are many studies which suggested the connection between periodontitis and systemic disease, however, the role of specific miRNA as a intersection of periontitis and diabetes are not elucidated. We suggested miR-25-3p as possible common mediator in the pathogenesis of periodontitis and diabetes.

2021-11-20 | GSE189107 | GEO

Chemerin-induced down-regulation of placenta-derived exo-somal miR-140-3p and miR-574-3p promotes umbilical vein endothelial cells proliferation, migration, and tube formation in gestational diabetes mellitus

Project description:Gestational diabetes mellitus (GDM) leads to poor pregnancy outcomes and fetoplacental endothelial dysfunction; however, the underlying mechanisms are still unknown. This study aimed to investigate the effect of placenta-derived exosomal miRNAs on fetoplacental endothelial dysfunction in GDM, and to further explore the role of chemerin to this end. Placenta-derived exosomal miR-140-3p and miR-574-3p expression (next-generation sequencing, quantitative real-time PCR), its interactions with cell function (Cell Counting Kit-8, Transwell, tube formation assay), chemerin interactions (Western blotting), and placental inflammation (immunofluorescence staining, enzyme-linked immunosorbent assay) were investigated. Placenta-derived exosomal miR-140-3p and miR-574-3p were downregulated in GDM. Additionally, miR-140-3p and miR-574-3p inhibited the proliferation, migration, and tube formation ability of umbilical vein endothelial cells by targeting vascular endothelial growth factor. Interestingly, miR-140-3p and miR-574-3p expression levels were negatively correlated with chemerin, which induced placental inflammation through the recruitment of macrophage cells and release of IL-18 and IL-1β. These findings indicate that chemerin reduces placenta-derived exosomal miR-140-3p and miR-574-3p levels by inducing placental inflammation, thereby promoting the proliferation, migration, and tube formation of umbilical vein endothelial cells in GDM, providing a novel perspective on the underlying pathogenesis and therapeutic targets for GDM and its offspring complications.

2022-11-16 | GSE213799 | GEO

RNA sequencing of RipmiR-141~200c and RipmiR-141~200c Zeb1200M islets

Project description:We performed RNA sequencing of islets of Langerhans isolated from RipmiR-141~200c and RipmiR-141~200c Zeb1200M mice to determine the transcriptomic effects of mutating miR-200 binding sites in the endogenous Zeb1 3'UTR of mice in which miR-141~200c is overexpressed under the rat insulin promoter (RIP).

2022-04-30 | E-MTAB-10537 | biostudies-arrayexpress

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