Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA576379 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10244600.fastq.gz | Fastqsanger.gz | |||
| SRR10244601.fastq.gz | Fastqsanger.gz | |||
| SRR10244602.fastq.gz | Fastqsanger.gz | |||
| SRR10244603.fastq.gz | Fastqsanger.gz | |||
| SRR10244604.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 72 |
Similar Datasets
Project description:The “nonclassic” apparent mineralocorticoid excess (NC-AME) has been identified in approximately 7% of general population. Our aim was to identify miRNAs within urinary exosomes associated to the NC-AME phenotype. A total of 18 urine samples (9 control and 9 NC-AME) derived from adult and children subjects were analyzed using small RNA sequencing.
2020-04-14 | GSE138556 | GEO
Project description:BACKGROUND:The "nonclassic" apparent mineralocorticoid excess (NC-AME) has been identified in approximately 7% of general population. This phenotype is characterized by low plasma renin activity (PRA), high serum cortisol (F) to cortisone (E) ratio, low cortisone, high Fractional Excretion of potassium (FEK) and normal-elevated systolic blood pressure (SBP). An early detection and/or identification of novel biomarkers of this phenotype could avoid the progression or future complications leading to arterial hypertension. Isolation of extracellular vesicles, such as exosomes, in specific biofluids support the identification of tissue-specific RNA and miRNA, which may be useful as novel biomarkers. Our aim was to identify miRNAs within urinary exosomes associated to the NC-AME phenotype. METHODS:We perform a cross-sectional study in a primary care cohort of 127 Chilean subjects. We measured BP, serum cortisol, cortisone, aldosterone, PRA. According to the previous reported, a subgroup of subjects was classified as NC-AME (n = 10). Urinary exosomes were isolated and miRNA cargo was sequenced by Illumina-NextSeq-500. RESULTS:We found that NC-AME subjects had lower cortisone (p < 0.0001), higher F/E ratio (p < 0.0001), lower serum potassium (p = 0.009) and higher FEK 24 h (p = 0.03) than controls. We found miR-204-5p (fold-change = 0.115; p 0.001) and miR-192-5p (fold-change = 0.246; p 0.03) are both significantly downregulated in NC-AME. miR-192-5p expression was correlated with PRA (r = 0.45; p 0.028) and miR-204-5p expression with SBP (r = - 0.48, p 0.027) and F/E ratio (r = - 0.48; p 0.026). CONCLUSIONS:These findings could support a potential role of these miRNAs as regulators and novel biomarkers of the NC-AME phenotype.
| S-EPMC6880399 | biostudies-literature
Project description:Small extracellular vesicles (sEVs) play a critical role in cardiac cell therapy by delivering molecular cargo and mediating cellular signaling. Among sEV cargo molecule types, microRNA (miRNA) is particularly potent and highly heterogenous. However, not all miRNAs in sEV are beneficial. Two previous studies utilizing computational modeling identified miR-192-5p and miR-432-5p as potentially deleterious in cardiac function and repair. Here, we show that knocking down miR-192-5p and miR-432-5p in cardiac c-kit+ cell-derived sEVs enhances the therapeutic capabilities of sEVs in vitro and in a rat in vivo model of cardiac ischemia reperfusion. miR-192-5p and miR-432-5p depleted CPC-sEVs enhance cardiac function by reducing fibrosis, enhancing mesenchymal stromal cell-like cell mobilization, and inducing macrophage polarization to the M2 phenotype. Knocking down deleterious miRNAs from sEV could be a promising therapeutic strategy for treatment of chronic myocardial infarction.
2022-12-31 | GSE196469 | GEO
Project description:Aldosterone controls sodium homeostasis by binding to the Mineralocorticoid Receptor (MR). We previously identified a specific temporal window during renal development when MR expression is low, explaining the physiological sodium losses observed in newborns at birth. However, underlying molecular mechanisms controlling MR expression remain unknown. Recently, we demonstrated in adult renal KC3AC1 cell line that MR expression is controlled by microRNAs (miR-30c-2-3p and miR-324-5p) in response to tonicity. Herein, we highlight the involvement of two microRNAs (miR-409-3p and miR-431-5p) in the regulation of MR expression during the neonatal period. RT-qPCR validated candidates microRNAs identified by high throughput screening approach and transfection of a luciferase reporter construct together with miRNAs Mimics or Inhibitors demonstrated their functional interaction with target transcripts. Underexpression strategies using Inhibitors revealed the impact on MR expression and signaling in primary culture renal cells. miR-409-3p and miR-431-5p are increased at D0 in mirror to MR expression. These miRNAs directly affect Nr3c2 (MR) transcript stability and enhances MR expression and signaling at D0. Whereas, overexpression strategies using Mimics, destabilize MR expression and mineralocorticoid signaling in primary culture renal cells at D8. We also confirm that their expression is increased in urine from neonates at birth, an expression that gradually decreased after birth (PREMALDO cohort). Finally, we performed an RNA sequencing to evaluate an integrative network of miRNAs and mRNA differentially expressed between D0 and D8. Differentially expressed genes (DEG) were crossed with the two candidate miRNAs, and 83 differentially expressed target genes (DETG) were obtained. Functional annotation suggested that kidney development and sodium transport/homeostasis pathways were significantly enriched. Our findings provide new predictive and non-invasive biomarkers of renal maturity and mineralocorticoid signaling expression and efficacy in human premature infants.
2025-02-10 | GSE275861 | GEO
Project description:Aldosterone controls sodium homeostasis by binding to the Mineralocorticoid Receptor (MR). We previously identified a specific temporal window during renal development when MR expression is low, explaining the physiological sodium losses observed in newborns at birth. However, underlying molecular mechanisms controlling MR expression remain unknown. Recently, we demonstrated in adult renal KC3AC1 cell line that MR expression is controlled by microRNAs (miR-30c-2-3p and miR-324-5p) in response to tonicity. Herein, we highlight the involvement of two microRNAs (miR-409-3p and miR-431-5p) in the regulation of MR expression during the neonatal period. RT-qPCR validated candidates microRNAs identified by high throughput screening approach and transfection of a luciferase reporter construct together with miRNAs Mimics or Inhibitors demonstrated their functional interaction with target transcripts. Underexpression strategies using Inhibitors revealed the impact on MR expression and signaling in primary culture renal cells. miR-409-3p and miR-431-5p are increased at D0 in mirror to MR expression. These miRNAs directly affect Nr3c2 (MR) transcript stability and enhances MR expression and signaling at D0. Whereas, overexpression strategies using Mimics, destabilize MR expression and mineralocorticoid signaling in primary culture renal cells at D8. We also confirm that their expression is increased in urine from neonates at birth, an expression that gradually decreased after birth (PREMALDO cohort). Finally, we performed an RNA sequencing to evaluate an integrative network of miRNAs and mRNA differentially expressed between D0 and D8. Differentially expressed genes (DEG) were crossed with the two candidate miRNAs, and 83 differentially expressed target genes (DETG) were obtained. Functional annotation suggested that kidney development and sodium transport/homeostasis pathways were significantly enriched. Our findings provide new predictive and non-invasive biomarkers of renal maturity and mineralocorticoid signaling expression and efficacy in human premature infants.
2025-02-10 | GSE275860 | GEO
Project description:This is a prospective-retrospective study to determine if the expression of the miRNA’s miR-31-3p and miR-31-5p are prognostic of patient outcomes or predictive of the benefit from anti-EGFR therapy in stage III Colon Cancer. The present study will utilize FFPE tumor samples collected from patients enrolled in the PETACC-8 study conducted by the Fédération Francophone de Cancérologie Digestive (FFCD). This phase 3 clinical trial prospectively randomized fully resected stage III colon cancer patients to receive adjuvant treatment with either FOLFOX-4 plus cetuximab or FLOFOX-4 alone.
| 2260465 | ecrin-mdr-crc
Project description:miR-493-5p, miR-3662, and miR-589-3p were estimated as working microRNAs in bleomycin- and methotrexate-induced phenotypic changes in A549 cells via microRNAs-Proteins Analysis of Integrative Relationship (miR-PAIR). To verify the effect of these miRNAs on the their target protein expression levels, comprehensive expression of proteins in A549 cells treated with miR-493-59, miR-3662, and miR-589-3p mimic was examined by SWATH-MS method. As expected by a miR-PAIR mehtod, almost target proteins were succesfully regulated by miR-493-5p and miR-589-3p mimics.
2025-07-25 | PXD053397 | Pride
Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.
2024-12-11 | PXD041087 | Pride
Project description:Post-transcriptional regulation of gene expression by miRNAs likely makes significant contributions to mRNA abundance at the embryo-maternal interface. In this study, we investigated how miR-26a-5p and miR-125b-5p contribute to molecular changes occurring in the uterine luminal epithelium, which serves as the first site of signal exchange between the mother and developing embryo. To measure de novo protein synthesis after miRNA delivery to primary uterine luminal epithelial cells, we employed pulsed stable isotope labeling by amino acids (pSILAC). We found that both miRNAs alter the proteome of luminal epithelial cells, impacting numerous cellular functions, immune responses, as well as intracellular and second messenger signaling pathways. Additionally, we identified several features of miRNA-mRNA interactions that may influence the targeting efficiency of miR-26a-5p and miR-125b-5p. Overall, our study suggests a complex interaction of miR-26a-5p and miR-125b-5p with their respective targets. However, both appear to cooperatively function in modulating the cellular environment of the luminal epithelium, facilitating the morphological and molecular changes that occur during the intensive communication between the embryo and uterus at pregnancy.
2025-05-07 | PXD056243 | Pride
Project description:Apparent Mineralocorticoid Excess Syndrome Natural History Clinical Protocol - RGSDC 5601
| PRJNA189541 | ENA