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    Neutrophil Gelatinase-Associated Lipocalin from immune cells is mandatory for aldosterone-induced cardiac remodeling and inflammation

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    item_2-s2.0-85040021182.pdf (4.180Kb)
    Date
    2018
    DOI
    10.1016/j.yjmcc.2017.12.011

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    Author
    Buonafine M.
    Martínez-Martínez E.
    Amador C.
    Gravez B.
    Ibarrola J.
    Fernández-Celis A.
    El Moghrabi S.
    Rossignol P.
    López-Andrés N.
    Jaisser F.
    Abstract
    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
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    LA UNIVERSIDAD
    • Aseguramiento de Calidad
    • Internacional
    • Vinculación con el Medio
    • Más Transparencia
    • Acreditación
    • Reglamentos e instructivos
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    FACULTADES
    • Administración y Negocios
    • Arquitectura y Construcción
    • Ciencias de la Salud
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    • Derecho
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    • Ingeniería
    INVESTIGACIÓN
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    • Postgrados
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