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Project description:The current study is aimed on determine the functional impact of microRNA-378a-3p and microRNA-146b on embryo development. For such purpose, we supplemented miR-378/miR-146b mimics or inhibitors to the culture medium containing presumed zygotes at 1 dpi and cultured them until day 8, thus allowing miR-378/miR-146b mimics or inhibitors to influence further embryo development and quality. Further on, to gain more in-depth molecular insights, we performed transcriptome profiling of blastocysts cultured in the presence of miR-378/miR-146b mimics or inhibitors.
2022-03-10 | GSE197876 | GEO
Project description:The current study is focused on Isolating EVs and their cargo content (miRNAs) from culture medium conditioned by individual embryos that can differentiate between the blastocyst and non-blastocyst embryos. We were able to isolate EVs from both blastocyst and non-blastocyst group with size exclusion chromatography (Izon’s™ qEV single column) and characterize them with Western blotting, nanoparticle tracking analysis, and Transmission electron microscopy. Further, we could isolate total RNA (including small RNAs) from the blastocyst and non-blastocyst EVs for miRNA sequencing.
2022-03-10 | GSE197875 | GEO
Project description:Hatching is modulated by microRNA-378a-3p derived from extracellular vesicles secreted by blastocysts
| PRJNA812556 | ENA
Project description:Hatching is modulated by microRNA-378a-3p derived from extracellular vesicles secreted by blastocysts (mRNA)
| PRJNA812576 | ENA
Project description:Hatching is modulated by microRNA-378a-3p derived from extracellular vesicles secreted by blastocysts (miRNA)
| PRJNA812577 | ENA
Project description:This study sought to determine whether mesenchymal stem cells-derived extracellular vesicles (MSCs-EVs) carrying microRNA-378a-3p (miR-378a-3p) could affect the pathogenesis of inflammatory bowel disease (IBD) by regulating the GATA-binding protein 2 (GATA2)/aquaporin-4 (AQP4)/peroxisome proliferator-activated receptor α (PPAR-α) axis. Initially, colon mucosa biopsy tissues were harvested from healthy controls and patients with IBD for qRT-PCR and immunohistochemistry analysis. EVs harvested from MSCs and lipopolysaccharide (LPS) were used to stimulate the M064 cells to establish an in vitro inflammation cell model. Besides, 2,4,6-trinitrobenzene sulfonic acid intracolon administration was performed to establish in vivo IBD mouse models. After loss- and gain-of-function assays, the regulatory role of MSCs-derived EVs loaded with manipulated miR-378a-3p in IBD in relation to GATA2/AQP4/PPAR-α were explored. Upregulation of GATA2 was identified in the colon tissue of IBD patients. GATA2, which was a target gene of miR-378a-3p, transcriptionally upregulated AQP4. After silencing of GATA2, LPS-induced apoptosis of M064 cells was reduced by the downregulation of AQP4. Decreased AQP4 contributed to PPAR-α pathway inactivation and weakened the LPS-induced apoptosis of M064 cells. MSCs-EVs delivering miR-378a-3p suppressed the GATA2/AQP4/PPAR-α pathway, which reduced LPS-induced apoptosis of M064 cells and the occurrence of IBD in mice. Altogether, the current study illustrated that MSCs-EVs transfer miR-378a-3p to reduce the GATA2 expression, which downregulates AQP4 to block the PPAR-α signalling pathway, thus suppressing the occurrence of IBD.
| S-EPMC9170824 | biostudies-literature
Project description:Extracellular vesicles (EVs) secreted from tumor-associated macrophages (TAMs) are known to generate an immune-suppressive environment conducive to the development of ovarian cancer (OC). We tried to elucidate the role of TAM-derived exosomal microRNA (miR)-29a-3p in OC. miR-29a-3p, forkhead box protein O3 (FOXO3), and programmed death ligand-1 (PD-L1) expression was determined and their interactions evaluated. EVs were isolated, followed by determination of the uptake of EVs by OC cells, after which the proliferation and immune escape facilities of the OC cells were determined. OC xenograft models were constructed with EVs in correspondence with in vivo experiments. Overexpressed miR-29a-3p was detected in OC, and miR-29a-3p promoted OC cell proliferation and immune escape. EVs derived from TAMs enhanced the proliferation of OC cells. miR-29a-3p was enriched in TAM-EVs, and TAM-EVs delivered miR-29a-3p into OC cells. Downregulated FOXO3 was identified in OC, whereas miR-29a-3p targeted FOXO3 to suppress glycogen synthase kinase 3β (GSK3β) activity via the serine/threonine protein kinase (AKT)/GSK3β pathway. Inhibition of TAM-derived exosomal miR-29a-3p decreased PD-L1 to inhibit OC progression through the FOXO3-AKT/GSK3β pathway in vitro and in vivo. Taken together, the current studies highlight the FOXO3-AKT/GSK3β pathway and the mechanism by which TAM-derived exosomal miR-29a-3p enhances the expression of PD-L1 to facilitate OC cell proliferation and immune escape.
| S-EPMC8463289 | biostudies-literature
Project description:Osteosarcoma (OS) is the most common primary bone cancer characterized by an aggressive phenotype with bone destruction. The prognosis of OS patients remains unoptimistic with the current treatment strategy. Recently, osteoclasts are believed to play a crucial role in cancer bone metastasis. Thus, osteoclast could be a target both in bone destruction and cancer progression in OS. However, mechanisms governing osteoclastogenesis in OS remain poorly understood. miRNA delivered by small extracellular vesicles (sEVs) could mediate cellular communications. In this study, we investigated the effects of sEVs on osteoclastogenesis and osteoclast function, also clarified the underlying mechanism. We herein found that sEVs promoted pre-osteoclast migration, osteoclastogenesis and resorption by exposing RAW264.7 cells to sEVs derived from OS cells. Bioinformatics analysis showed that phosphatase tension homologue (PTEN), and miR-19a-3p were involved in OS progression. Overexpression of miR-19a-3p or sEVs' miR-19a-3p promoted osteoclast formation and function through PTEN/PI3K/AKT signaling pathway, while inhibition of miR-19a-3p showed the contrary results. The bone marrow macrophages (BMMs) were used to verify the results. OS mice, which were established by subcutaneous injection of OS cells, exhibited increased levels of sEVs' miR-19a-3p in blood. Moreover, micro-computed tomography (CT) and histomorphometry analysis demonstrated that OS mice exhibited osteopenia with increased number of osteoclasts. In conclusion, miR-19a-3p delivery via OS cell-derived sEVs promotes osteoclast differentiation and bone destruction through PTEN/phosphatidylinositol 3 -kinase (PI3K)/protein kinase B (AKT) signaling pathway. These findings highlight sEVs packaging of miR-19a-3p as a potential target for prevention and treatment of bone destruction and cancer progression in OS patients. And this finding provides a novel potentially therapeutic target for the bone metastasis.
| S-EPMC8029976 | biostudies-literature
Project description:Background Extracellular vesicles (EVs) are a popular treatment candidate for myocardial injury. This work investigated the effects of mesenchymal stem cells (MSCs)-secreted EVs-derived miR-200b-3p on cardiomyocyte apoptosis and inflammatory response after myocardial infarction (MI) through targeting BCL2L11 (Bcl-2-like protein 11) . Methods and Results EVs from MSCs were isolated and identified. EVs from MSCs with transfection of miR-200b-3p for overexpression were injected into MI mice. The effect of miR-200b-3p on cardiac function, infarction area, myocardial fibrosis, cardiomyocyte apoptosis, and inflammatory response was determined in MI mice. The targeting relationship between miR-200b-3p and BCL2L11 was verified, and the interaction between BCL2L11 and NLR family pyrin domain containing 1 (NLRP1) was also verified. MI mice were injected with an overexpressing BCL2L11 lentiviral vector to clarify whether BCL2L11 can regulate the effect of miR-200b-3p on MI mice. EVs from MSCs were successfully extracted. MSCs-EVs improved cardiac function and reduced infarction area, apoptosis of cardiomyocytes, myocardial fibrosis, and inflammation in MI mice. Upregulation of miR-200b-3p further enhanced the effects of MSCs-EVs on the myocardial injury of MI mice. BCL2L11 was targeted by miR-200b-3p and bound to NLRP1. Upregulation of BCL2L11 negated the role of miR-200b-3p-modified MSCs-EVs in MI mice. Conclusions A summary was obtained that miR-200b-3p-encapsulated MSCs-EVs protect against MI-induced apoptosis of cardiomyocytes and inflammation via suppressing BCL2L11.
| S-EPMC9238663 | biostudies-literature
Project description:Atherosclerosis has been regarded as a major contributor to cardiovascular disease. The role of extracellular vesicles (EVs) in the treatment of atherosclerosis has been increasingly reported. In this study, we set out to investigate the effect of macrophages-derived EVs (M-EVs) containing miR-19b-3p in the progression of atherosclerosis, with the involvement of JAZF1. Following isolation of EVs from macrophages, the M-EVs were induced with ox-low density lipoprotein (LDL) (ox-LDL-M-EVs), and co-cultured with vascular smooth muscle cells (VSMCs). RT-qPCR and western blot assay were performed to determine the expression of miR-19b-3p and JAZF1 in M-EVs and in VSMCs. Lentiviral infection was used to overexpress or knock down miR-19b-3p. EdU staining and scratch test were conducted to examine VSMC proliferation and migration. Dual-luciferase gene reporter assay was performed to examine the relationship between miR-19b-3p and JAZF1. In order to explore the role of ox-LDL-M-EVs carrying miR-19b-3p in atherosclerotic lesions in vivo, a mouse model of atherosclerosis was established through high-fat diet induction. M-EVs were internalized by VSMCs. VSMC migration and proliferation were promoted by ox-LDL-M-EVs. miR-19b-3p displayed upregulation in ox-LDL-M-EVs. miR-19b-3p was transferred by M-EVs into VSMCs, thereby promoting VSMC migration and proliferation. mir-19b-3p targeted JAZF1 to decrease its expression in VSMCs. Atherosclerosis lesions were aggravated by ox-LDL-M-EVs carrying miR-19b-3p in ApoE-/- mice. Collectively, this study demonstrates that M-EVs containing miR-19b-3p accelerate migration and promotion of VSMCs through targeting JAZF1, which promotes the development of atherosclerosis.
| S-EPMC8742201 | biostudies-literature