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

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

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE241242 | 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 [exosome-miR-seq]

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

2023-08-25 | GSE241241 | 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.

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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

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

| PRJNA1007565 | ENA

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]

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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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Protective cellular mechanism of estrogen against kidney stone formation: A proteomics approach and functional validation

Project description:Kidney stone disease is influenced by multiple factors, including but not limited to age, gender, genetic background, hydration status, diet and drug. Regarding the gender, epidemiologic data across the world has shown that females at the reproductive age (15-49 years) have lower incidence/prevalence of kidney stone disease approximately 1.5-2.5 folds as compared to males at the same age. However, this gap is narrower in the postmenopausal age, whereas the postmenopausal females with higher serum estrogen levels are less likely to have kidney stones. Furthermore, female stone formers (patients with kidney stones) are associated with lower estrogen levels. Therefore, estrogen has been proposed to serve as the protective hormone against kidney stone disease. However, the precise mechanisms underlying such protective effects of estrogen remain unclear and require further investigations. This study thus investigated the effects of estradiol (which is the most prevalent and potent form of estrogen in females at the reproductive age) on cellular proteome of renal tubular cells using a proteomics approach.

2019-09-09 | PXD014768 | Pride

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