Evidence map›Paper›PMID 31775784›Full record

ArticleJournal of translational medicine2019

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

Alejandra Tapia-Castillo, Dominic Guanzon, Carlos Palma, Andrew Lai, Eric Barros, Fidel Allende, Andrea Vecchiola, Carlos E Fardella, Carlos Salomón, Cristian A Carvajal

Abstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Role of microRNAs in Obesity-Related Kidney Disease.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Observational
  11. Article
  12. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Alejandra Tapia-CastilloDepartment of Endocrinology, School of Medicine, Pontificia Universidad Católica de Chile, Diagonal Paraguay 362, piso 4, Santiago, 8330077, Chile.
Dominic GuanzonExosome Biology Laboratory, Centre for Clinical Diagnostics, University of Queensland Centre for Clinical Research, Royal Brisbane and Women's Hospital, The University of Queensland, Brisbane, QLD, 4029, Australia.
Carlos PalmaExosome Biology Laboratory, Centre for Clinical Diagnostics, University of Queensland Centre for Clinical Research, Royal Brisbane and Women's Hospital, The University of Queensland, Brisbane, QLD, 4029, Australia.
Andrew LaiExosome Biology Laboratory, Centre for Clinical Diagnostics, University of Queensland Centre for Clinical Research, Royal Brisbane and Women's Hospital, The University of Queensland, Brisbane, QLD, 4029, Australia.
Eric BarrosDepartment of Endocrinology, School of Medicine, Pontificia Universidad Católica de Chile, Diagonal Paraguay 362, piso 4, Santiago, 8330077, Chile.
Fidel AllendeCentro Traslacional de Endocrinología (CETREN-UC), Pontificia Universidad Católica de Chile, Santiago, Chile.
Andrea VecchiolaDepartment of Endocrinology, School of Medicine, Pontificia Universidad Católica de Chile, Diagonal Paraguay 362, piso 4, Santiago, 8330077, Chile.
Carlos E FardellaDepartment of Endocrinology, School of Medicine, Pontificia Universidad Católica de Chile, Diagonal Paraguay 362, piso 4, Santiago, 8330077, Chile.
Carlos SalomónExosome Biology Laboratory, Centre for Clinical Diagnostics, University of Queensland Centre for Clinical Research, Royal Brisbane and Women's Hospital, The University of Queensland, Brisbane, QLD, 4029, Australia.
Cristian A CarvajalDepartment of Endocrinology, School of Medicine, Pontificia Universidad Católica de Chile, Diagonal Paraguay 362, piso 4, Santiago, 8330077, Chile. ccarvajm@uc.cl.ORCID 0000-0002-0668-412X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe "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.

methodsWe 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.

resultsWe 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).

conclusionsThese findings could support a potential role of these miRNAs as regulators and novel biomarkers of the NC-AME phenotype.

Indexed as

AdolescentAdultCase-Control StudiesChildDown-RegulationExosomesFemaleHumansMaleMicroRNAsMiddle AgedMineralocorticoid Excess Syndrome, ApparentReproducibility of ResultsYoung AdultMicroRNAsMIRN192 microRNA, humanMIRN204 microRNA, humanExosomesHypertensionMicroRNAMineralocorticoid receptorNonclassic AME

Identifiers

PMID31775784
PMCPMC6880399

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.