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Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess

ABSTRACT: Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess

PROVIDER: PRJNA576379 | ENA |

REPOSITORIES: ENA

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			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

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Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess

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

Downregulation of exosomal miR-192-5p and miR-204-5p in subjects with nonclassic apparent mineralocorticoid excess.

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.

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Knockdown of miR-192 and miR-432 in progenitor cell-derived small extracellular vesicles enhances tissue repair in myocardial infarction

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.

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2023-12-31 | GSE235075 | GEO

Coordinated regulation of cell cycle transcripts by p53-inducible microRNAs, miR -192 and -215

Project description:Cell cycle arrest in response to DNA damage is an important anti-tumorigenic mechanism. microRNAs (miRNAs) were shown recently to play key regulatory roles in cell cycle progression. For example, miR-34a is induced in response to p53 activation and mediates G1 arrest by down-regulating multiple cell cycle-related transcripts. Here we show that genotoxic stress promotes the p53-dependent up-regulation of the homologous miRNAs, miR -192 and miR-215. Like miR-34a, activation of miR-192/215 induces cell cycle arrest suggesting that multiple microRNA families operate in the p53 network. Furthermore, we define a downstream gene expression signature for miR-192/215 expression that includes a number of transcripts that regulate G1 and G2 checkpoints. Of these transcripts, 18 transcripts are direct targets of miR-192/215 and the observed cell cycle arrest likely results from a cooperative effect among the modulations of these genes by the miRNAs. Our results demonstrating a role for miR-192/215 in cell proliferation combined with recent observations that these miRNAs are under-expressed in primary cancers support the idea that miR-192 and miR-215 function as tumor-suppressors.

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Microarray of K562 cell line after overexpression of miR-15a-5p or miR-21-5p.

Project description:The aim was to look for target genes of miR-15a-5p or miR-21-5p.

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Coordinated regulation of cell cycle transcripts by p53-inducible microRNAs, miR -192 and -215

2010-06-24 | E-GEOD-13105 | biostudies-arrayexpress