Evidence map›Paper›PMID 31165585›Full record

ArticlePhysiological reports2019

Both aldosterone and spironolactone can modulate the intracellular ACE/ANG II/AT1 and ACE2/ANG (1-7)/MAS receptor axes in human mesangial cells.

Danielle Stoll, Rodrigo Yokota, Danielle Sanches Aragão, Dulce E Casarini

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  8. Coronary microvascular dysfunction pathophysiology in COVID-19.Microcirculation (New York, N.Y. : 1994) · 2021
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  13. DNA Methylation of the Angiotensinogen Gene,International journal of molecular sciences · 2021
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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

4 authors at 1 institution in 1 country.

Danielle StollEscola Paulista de Medicina - Department of Medicine, Nephrology Division, Universidade Federal de São Paulo, UNIFESP, São Paulo, Brazil.
Rodrigo YokotaEscola Paulista de Medicina - Department of Medicine, Nephrology Division, Universidade Federal de São Paulo, UNIFESP, São Paulo, Brazil.
Danielle Sanches AragãoEscola Paulista de Medicina - Department of Medicine, Nephrology Division, Universidade Federal de São Paulo, UNIFESP, São Paulo, Brazil.
Dulce E CasariniEscola Paulista de Medicina - Department of Medicine, Nephrology Division, Universidade Federal de São Paulo, UNIFESP, São Paulo, Brazil.ORCID 0000-0003-1912-4292
Universidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kidney is an important target of the renin-ANG-aldosterone system (RAAS). To date, several studies have demonstrated the existence of a local RAAS in various tissues, including the renal tissue. The mineralocorticoid aldosterone is known to play a critical role in the classical RAAS; however, its effect on mesangial cells (MCs) remains to be elucidated. Based on this, our aim was to investigate whether aldosterone stimulation can modulate the intracellular RAAS of immortalized human MCs by evaluating ANG-converting enzyme (ACE)/ANG II/ANG II receptor type 1 (AT1) and ANG-converting enzyme 2 (ACE2)/ANG (1-7)/MAS receptor axes. To realise this, protein expression, enzyme activity, and immunofluorescence were performed under aldosterone stimulation and in the presence of the mineralocorticoid receptor (MR) antagonist spironolactone (SPI). We observed that high doses of aldosterone increase ACE activity. The effect of aldosterone on the catalytic activity of ACE was completely abolished with the pretreatment of SPI suggesting that the aldosterone-induced cell injuries through ANG II release were attenuated. Aldosterone treatment also decreased the expression of MAS receptor, but did not alter the expression or the catalytic activity of ACE 2 and ANG (1-7) levels. Spironolactone modulated the localization of ANG II and AT1 receptor and decreased ANG (1-7) and MAS receptor levels. Our data suggest that both aldosterone and the MR receptor antagonist can modulate both of these axes and that spironolactone can protect MCs from the damage induced by aldosterone.

Indexed as

AldosteroneAngiotensin-Converting Enzyme 2Angiotensin ICells, CulturedGlycosylationHumansMesangial CellsMineralocorticoid Receptor AntagonistsPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptor, Angiotensin, Type 1Receptors, G-Protein-CoupledSpironolactoneVesicular Transport ProteinsACE2 protein, humanACE protein, humanAldosteroneAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Mineralocorticoid Receptor AntagonistsPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptor, Angiotensin, Type 1Receptors, G-Protein-CoupledSpironolactoneVesicular Transport ProteinsVPS51 protein, humanAldosteronemesangial cellsrenin-ANG-aldosterone systemspironolactone

Identifiers

PMID31165585
PMCPMC6548847
OpenAlexW2948840404

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.