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MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling [exosome-miR-seq]

ABSTRACT: To investigate the potential role of miRNA-148b-5p in the pathogenesis of kidney stones, we conducted urinary exosomal sequencing.

ORGANISM(S): Homo sapiens

PROVIDER: GSE241241 | GEO | 2023/08/25

REPOSITORIES: GEO

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MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling [RIP-seq]

Project description:To investigate the potential role of miRNA-148b-5p in the pathogenesis of kidney stones, we conducted RIP-seq of rat's kidney tissue.

2023-08-25 | GSE241242 | GEO

MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-25 | GSE241243 | GEO

MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling [exosome-miR-seq]

Project description:MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling [exosome-miR-seq]

| PRJNA1007566 | ENA

MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling

Project description:MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling

| PRJNA1007564 | ENA

MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling [RIP-seq]

Project description:MiR-148b-5p promotes hypercalciuric kidney stone formation via regulating circRNA-83536/miR-24-3p/Calcitonin Receptor signaling [RIP-seq]

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miR-148b modulates the expression of multiple genes

Project description:To identify which miR-148b targets were involved in tumorigenesis, a microarray analysis was performed for miR-148b over-expressing cells versus controls and 129 (49 up and 80 down) modulated genes were revealed. The effects of miR-148b on cancer progression depend on the direct and indirect regulation of multiple target genes. To identify miR-148b modulated genes, MDA-MB-231 cells were transfected with miR-148b precursors or negative controls (pre-miR-148b or control) and used 48h later for microarray and western blot (WB) analyses. When a âWhole Human Genome Oligo Microarrayâ (Agilent) platform was employed, 129 differentially expressed genes (49 upregulated, 80 downmodulated) were found at 48h, considering a fold change (FC) cut of 1.5 and a false discovery rate (FDR) of 16% (Table S4). Crossing these results with the list of putative miR-148b targets (3642) obtained by the miRecords System, we observed that 33 of the modulated genes were also miR-148b predicted targets and interestingly, 26 out of these 33 genes were downmodulated.

2012-12-16 | E-GEOD-26662 | biostudies-arrayexpress

miR-148b modulates the expression of multiple genes

2012-12-16 | GSE26662 | GEO

miR-148b modulates the C1GALT1 expression explaining the abnormal glycosylation process in IgA Nephropathy

Project description:Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide characterized by aberrant O-glycosylation in the hinge region of IgA1. The basis for the abnormal glycosylation in IgAN is still unknown, but an important involvement of the enzyme core 1, beta 1,3-galactosyltransferase 1 (C1GALT1) is known. However, the role of microRNAs (miRNAs), a new family of key mRNA regulatory molecules, in the IgAN pathogenesis has not yet been reported. In this study, by high-throughput microRNA profiling, we identified 37 miRNAs differentially expressed in peripheral blood mononuclear cells (PBMCs) from IgAN patients compared to healthy subjects. Among them, upregulated miR-148b potentially targeted C1GALT1, INVS and PTEN, three genes notably downregulated in IgAN patients. C1GALT1 expression levels in IgAN patients were reduced and negatively correlated with the upregulated miR-148b expression. We demonstrated the biological relationship between miR-148b and C1GALT1 by transient transfection experiments ex vivo. When we reduced the upregulated miR-148b function in PBMCs of IgAN patients an increase of the C1GALT1 mRNA and protein levels was observed. We validated biologically also the miR-148b targeting of INVS , involved in the altered modulation of the WNT–β-catenin and PI3K/Akt pathways in IgAN patients. All together our data evidence an important role of miR-148b in the pathogenesis of IgAN, which could explain the aberrant glycosylation of IgA1 in the pathogenesis and should light on a potential target for the theraphy of the disease.

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Exosome-Derived miR-25-3p and miR-92a-3p Stimulate Liposarcoma Progression.

Project description:Despite the development of combined modality treatments against liposarcoma in recent years, a significant proportion of patients respond only modestly to such approaches, possibly contributing to local or distant recurrence. Early detection of recurrent or metastatic disease could improve patient prognosis by triggering earlier clinical intervention. However, useful biomarkers for such purposes are lacking. Using both patient plasma samples and cell lines, we demonstrate here that miR-25-3p and miR-92a-3p are secreted by liposarcoma cells through extracellular vesicles and may be useful as potential biomarkers of disease. Both miR-25-3p and miR-92a-3p stimulated secretion of proinflammatory cytokine IL6 from tumor-associated macrophages in a TLR7/8-dependent manner, which in turn promoted liposarcoma cell proliferation, invasion, and metastasis via this interaction with the surrounding microenvironment. Our findings provide novel and previously unreported insight into liposarcoma progression, identifying communication between liposarcoma cells and their microenvironment as a process critically involved in liposarcoma progression. This study establishes the possibility that the pattern of circulating miRNAs may identify recurrence prior to radiological detectability while providing insight into disease outcome and as a possible approach to monitor treatment efficacy. Cancer Res; 77(14); 3846-56. ©2017 AACR.

| S-EPMC6033276 | biostudies-literature

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