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dc.contributor.authorBuonafine M.
dc.contributor.authorMartínez-Martínez E.
dc.contributor.authorAmador C.
dc.contributor.authorGravez B.
dc.contributor.authorIbarrola J.
dc.contributor.authorFernández-Celis A.
dc.contributor.authorEl Moghrabi S.
dc.contributor.authorRossignol P.
dc.contributor.authorLópez-Andrés N.
dc.contributor.authorJaisser F.
dc.date.accessioned2020-09-02T22:13:34Z
dc.date.available2020-09-02T22:13:34Z
dc.date.issued2018
dc.identifier10.1016/j.yjmcc.2017.12.011
dc.identifier.citation115, , 32-38
dc.identifier.issn00222828
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3800
dc.descriptionImmune system activation is involved in cardiovascular (CV) inflammation and fibrosis, following activation of the mineralocorticoid receptor (MR). We previously showed that Neutrophil Gelatinase-Associated Lipocalin (NGAL) is a novel target of MR signaling in CV tissue and plays a critical role in aldosterone/MR-dependent hypertension and fibrosis. We hypothesized that the production of NGAL by immune cells may play an important part in the mediation of these deleterious mineralocorticoid-induced effects. We analyzed the effect of aldosterone on immune cell recruitment and NGAL expression in vivo. We then studied the role of NGAL produced by immune cells in aldosterone-mediated cardiac inflammation and remodeling using mice depleted for NGAL in their immune cells by bone marrow transplantation and subjected to mineralocorticoid challenge NAS (Nephrectomy, Aldosterone 200 μg/kg/day, Salt 1%). NAS treatment induced the recruitment of various immune cell populations to lymph nodes (granulocytes, B lymphocytes, activated CD8 + T lymphocytes) and the induction of NGAL expression in macrophages, dendritic cells, and PBMCs. Mice depleted for NGAL in their immune cells were protected against NAS-induced cardiac remodeling and inflammation. We conclude that NGAL produced by immune cells plays a pivotal role in cardiac damage under mineralocorticoid excess. Our data further stressed a pathogenic role of NGAL in cardiac damages, besides its relevance as a biomarker of renal injury. © 2017
dc.language.isoen
dc.publisherAcademic Press
dc.subjectAldosterone
dc.subjectCardiovascular
dc.subjectFibrosis
dc.subjectInflammation
dc.subjectMR
dc.subjectNGAL
dc.subjectaldosterone
dc.subjectmineralocorticoid
dc.subjectneutrophil gelatinase associated lipocalin
dc.subjectaldosterone
dc.subjectneutrophil gelatinase associated lipocalin
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectB lymphocyte
dc.subjectbone marrow transplantation
dc.subjectcarditis
dc.subjectCD8+ T lymphocyte
dc.subjectcell selection
dc.subjectcontrolled study
dc.subjectdendritic cell
dc.subjectfibroblast
dc.subjectflow cytometry
dc.subjectgranulocyte
dc.subjectheart injury
dc.subjectheart muscle fibrosis
dc.subjectheart ventricle remodeling
dc.subjectimmunocompetent cell
dc.subjectin vivo study
dc.subjectkidney injury
dc.subjectlymph node
dc.subjectmacrophage
dc.subjectmale
dc.subjectmouse
dc.subjectnephrectomy
dc.subjectnonhuman
dc.subjectperipheral blood mononuclear cell
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectanimal
dc.subjectC57BL mouse
dc.subjectcardiac muscle
dc.subjectcell culture
dc.subjectcell proliferation
dc.subjectfibrosis
dc.subjectheart atrium remodeling
dc.subjecthuman
dc.subjectinflammation
dc.subjectknockout mouse
dc.subjectleukocyte
dc.subjectmetabolism
dc.subjectoxidative stress
dc.subjectpathology
dc.subjectAldosterone
dc.subjectAnimals
dc.subjectAtrial Remodeling
dc.subjectCell Proliferation
dc.subjectCells, Cultured
dc.subjectFibroblasts
dc.subjectFibrosis
dc.subjectHumans
dc.subjectInflammation
dc.subjectLeukocytes
dc.subjectLipocalin-2
dc.subjectMale
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMyocardium
dc.subjectNephrectomy
dc.subjectOxidative Stress
dc.titleNeutrophil Gelatinase-Associated Lipocalin from immune cells is mandatory for aldosterone-induced cardiac remodeling and inflammation
dc.typeArticle


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