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Neutrophil Gelatinase-Associated Lipocalin from immune cells is mandatory for aldosterone-induced cardiac remodeling and inflammation
dc.contributor.author | Buonafine M. | |
dc.contributor.author | Martínez-Martínez E. | |
dc.contributor.author | Amador C. | |
dc.contributor.author | Gravez B. | |
dc.contributor.author | Ibarrola J. | |
dc.contributor.author | Fernández-Celis A. | |
dc.contributor.author | El Moghrabi S. | |
dc.contributor.author | Rossignol P. | |
dc.contributor.author | López-Andrés N. | |
dc.contributor.author | Jaisser F. | |
dc.date.accessioned | 2020-09-02T22:13:34Z | |
dc.date.available | 2020-09-02T22:13:34Z | |
dc.date.issued | 2018 | |
dc.identifier | 10.1016/j.yjmcc.2017.12.011 | |
dc.identifier.citation | 115, , 32-38 | |
dc.identifier.issn | 00222828 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/3800 | |
dc.description | Immune 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.iso | en | |
dc.publisher | Academic Press | |
dc.subject | Aldosterone | |
dc.subject | Cardiovascular | |
dc.subject | Fibrosis | |
dc.subject | Inflammation | |
dc.subject | MR | |
dc.subject | NGAL | |
dc.subject | aldosterone | |
dc.subject | mineralocorticoid | |
dc.subject | neutrophil gelatinase associated lipocalin | |
dc.subject | aldosterone | |
dc.subject | neutrophil gelatinase associated lipocalin | |
dc.subject | animal cell | |
dc.subject | animal experiment | |
dc.subject | animal model | |
dc.subject | animal tissue | |
dc.subject | Article | |
dc.subject | B lymphocyte | |
dc.subject | bone marrow transplantation | |
dc.subject | carditis | |
dc.subject | CD8+ T lymphocyte | |
dc.subject | cell selection | |
dc.subject | controlled study | |
dc.subject | dendritic cell | |
dc.subject | fibroblast | |
dc.subject | flow cytometry | |
dc.subject | granulocyte | |
dc.subject | heart injury | |
dc.subject | heart muscle fibrosis | |
dc.subject | heart ventricle remodeling | |
dc.subject | immunocompetent cell | |
dc.subject | in vivo study | |
dc.subject | kidney injury | |
dc.subject | lymph node | |
dc.subject | macrophage | |
dc.subject | male | |
dc.subject | mouse | |
dc.subject | nephrectomy | |
dc.subject | nonhuman | |
dc.subject | peripheral blood mononuclear cell | |
dc.subject | priority journal | |
dc.subject | protein expression | |
dc.subject | protein function | |
dc.subject | animal | |
dc.subject | C57BL mouse | |
dc.subject | cardiac muscle | |
dc.subject | cell culture | |
dc.subject | cell proliferation | |
dc.subject | fibrosis | |
dc.subject | heart atrium remodeling | |
dc.subject | human | |
dc.subject | inflammation | |
dc.subject | knockout mouse | |
dc.subject | leukocyte | |
dc.subject | metabolism | |
dc.subject | oxidative stress | |
dc.subject | pathology | |
dc.subject | Aldosterone | |
dc.subject | Animals | |
dc.subject | Atrial Remodeling | |
dc.subject | Cell Proliferation | |
dc.subject | Cells, Cultured | |
dc.subject | Fibroblasts | |
dc.subject | Fibrosis | |
dc.subject | Humans | |
dc.subject | Inflammation | |
dc.subject | Leukocytes | |
dc.subject | Lipocalin-2 | |
dc.subject | Male | |
dc.subject | Mice, Inbred C57BL | |
dc.subject | Mice, Knockout | |
dc.subject | Myocardium | |
dc.subject | Nephrectomy | |
dc.subject | Oxidative Stress | |
dc.title | Neutrophil Gelatinase-Associated Lipocalin from immune cells is mandatory for aldosterone-induced cardiac remodeling and inflammation | |
dc.type | Article |