Aldosterone induces renal fibrosis and inflammatory M1-macrophage bubtype via mineralocorticoid receptor in rats
Entity
UAM. Departamento de Anatomía Patológica; UAM. Departamento de Medicina; Instituto de Investigación Sanitaria Fundación Jiménez Díaz (IIS-FJD)Publisher
Public Library of ScienceDate
2016-01-05Citation
10.1371/journal.pone.0145946
PLoS ONE 11.1 (2016): e0145946
ISSN
1932-6203DOI
10.1371/journal.pone.0145946Funded by
This work has been supported by grants from Fondo de Investigaciones Sanitaria (FIS, Programa Miguel Servet: CP10/00479, PI13/00802 and PI14/00883), Spanish Society of Nephrology to Juan Antonio Moreno, Fundación Conchita Rabago to Alfonso Rubio-Navarro, Institute of Research Queen Sophia, Fundacion Renal Iñigo Alvarez de Toledo (FRIAT) and Instituto de Salud Carlos III (ISCIII) fund PI14/00386 to Jesús Egido and VI Programa Nacional de Investigación Científica, Desarrollo e Innovación Tecnológica de España (SAF2011-30396).Project
Gobierno de España. SAF2011-30396Editor's Version
http://dx.doi.org/10.1371/journal.pone.0145946Subjects
Renal fibrosis; Inflammatory alterations; MedicinaRights
© 2016 Martín-Fernández et al.Abstract
We aimed to evaluate macrophages heterogeneity and structural, functional and inflammatory
alterations in rat kidney by aldosterone + salt administration. The effects of treatment
with spironolactone on above parameters were also analyzed. Male Wistar rats received
aldosterone (1 mgkg-1d-1) + 1% NaCl for 3 weeks. Half of the animals were treated with spironolactone
(200 mg kg-1d-1). Systolic and diastolic blood pressures were elevated (p<0.05)
in aldosterone + salt–treated rats. Relative kidney weight, collagen content, fibronectin,
macrophage infiltrate, CTGF, Col I, MMP2, TNF-α, CD68, Arg2, and SGK-1 were increased
(p<0.05) in aldosterone + salt–treated rats, being reduced by spironolactone (p<0.05).
Increased iNOS and IFN-γ mRNA gene expression (M1 macrophage markers) was
observed in aldosterone + salt rats, whereas no significant differences were observed in IL-
10 and gene ArgI mRNA expression or ED2 protein content (M2 macrophage markers). All
the observed changes were blocked with spironolactone treatment. Macrophage depletion
with liposomal clodronate reduced macrophage influx and inflammatory M1 markers (INF-γ
or iNOS), whereas interstitial fibrosis was only partially reduced after this intervention, in
aldosterone plus salt-treated rats. In conclusion, aldosterone + salt administration mediates
inflammatory M1 macrophage phenotype and increased fibrosis throughout mineralocorticoid
receptors activation
Files in this item
Google Scholar:Martín-Fernández, Beatriz
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Rubio-Navarro, Alfonso
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Cortegano, Isabel
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Ballesteros, Sandra
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Alía, Mario
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Cannata, Pablo
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Olivares-Álvaro, Elena
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Egido, Jesús
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Andrés, Belén de
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Gaspar, María Luisa
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Heras, Natalia de las
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Lahera, Vicente
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Moreno, Juan Antonio
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