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Dendritic cells are crucial for cardiovascular remodeling and modulate neutrophil gelatinase-associated lipocalin expression upon mineralocorticoid receptor activation

dc.contributor.authorAraos P.
dc.contributor.authorPrado C.
dc.contributor.authorLozano M.
dc.contributor.authorFigueroa S.
dc.contributor.authorEspinoza A.
dc.contributor.authorBerger T.
dc.contributor.authorMak T.W.
dc.contributor.authorJaisser F.
dc.contributor.authorPacheco R.
dc.contributor.authorMichea L.
dc.contributor.authorAmador C.A.
dc.date.accessioned2020-09-02T22:12:22Z
dc.date.available2020-09-02T22:12:22Z
dc.date.issued2019
dc.identifier10.1097/HJH.0000000000002067
dc.identifier.citation37, 7, 1482-1492
dc.identifier.issn02636352
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3579
dc.descriptionBackground:Adaptive immunity is crucial in cardiovascular and renal inflammation/fibrosis upon hyperactivation of mineralocorticoid receptor. We have previously demonstrated that dendritic cells can respond to mineralocorticoid receptor activation, and the neutrophil gelatinase-associated lipocalin (NGAL) in dendritic cells is highly increased during aldosterone (Aldo)/mineralocorticoid receptor-dependent cardiovascular damage. However, the interrelationship among dendritic cells, target organs inflammation/fibrosis induced by mineralocorticoid receptor, and NGAL-dependence remains unknown.Objective:We studied the role of dendritic cells in mineralocorticoid receptor-dependent tissue remodeling and whether NGAL can modulate the inflammatory response of dendritic cells after mineralocorticoid receptor activation.Methods:Cardiovascular and renal remodeling induced by Aldo and high-salt diet [nephrectomy-Aldo-salt (NAS) model] were analyzed in CD11c.DOG mice, a model which allows dendritic cells ablation by using diphtheria toxin. In addition, in-vitro studies in NGAL-knock out dendritic cells were performed to determine the immunomodulatory role of NGAL upon Aldo treatment.Results:The ablation of dendritic cells prevented the development of cardiac hypertrophy, perivascular fibrosis, and the overexpression of NGAL, brain natriuretic peptide, and two profibrotic factors induced by NAS: collagen 1A1 and connective tissue growth factor. We determined that dendritic cells were not required to prevent renal hypertrophy/fibrosis induced by NAS. Between different immune cells analyzed, we observed that NGAL abundance was higher in antigen-presenting cells, while in-vitro studies showed that mineralocorticoid receptor stimulation in dendritic cells favored NGAL and IL-23 expression (p19 and p40 subunits), which are involved in the development of fibrosis and the Th17-driven response, respectively.Conclusion:NGAL produced by dendritic cells may play a pivotal role in the activation of adaptive immunity that leads to cardiovascular fibrosis during mineralocorticoids excess. © 2019 Wolters Kluwer Health, Inc. All rights reserved.
dc.language.isoen
dc.publisherLippincott Williams and Wilkins
dc.subjectcardiovascular fibrosis
dc.subjectdendritic cells
dc.subjectinflammation
dc.subjectmineralocorticoid receptor
dc.subjectneutrophil gelatinase-associated lipocalin
dc.subjectaldosterone
dc.subjectAPC protein
dc.subjectbrain natriuretic peptide
dc.subjectCD11b antigen
dc.subjectCD3 antigen
dc.subjectCD4 antibody
dc.subjectCD4 antigen
dc.subjectcollagen
dc.subjectcollagen 1a1
dc.subjectconnective tissue growth factor
dc.subjectdiphtheria toxin
dc.subjectgamma interferon
dc.subjectglycoprotein p 15095
dc.subjectgranulocyte macrophage colony stimulating factor
dc.subjectinterleukin 17
dc.subjectinterleukin 23
dc.subjectinterleukin 6
dc.subjectmineralocorticoid receptor
dc.subjectneutrophil gelatinase associated lipocalin
dc.subjectprotein p19
dc.subjectprotein p40
dc.subjectunclassified drug
dc.subjectbrain natriuretic peptide
dc.subjectCD11 antigen
dc.subjectIl23a protein, mouse
dc.subjectinterleukin 23p19
dc.subjectItgax protein, mouse
dc.subjectLcn2 protein, mouse
dc.subjectmineralocorticoid receptor
dc.subjectneutrophil gelatinase associated lipocalin
dc.subjectNr3c2 protein, mouse
dc.subjectadaptive immunity
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectantigen presenting cell
dc.subjectArticle
dc.subjectcardiovascular disease
dc.subjectcontrolled study
dc.subjectdendritic cell
dc.subjectenzyme activation
dc.subjectfemale
dc.subjectgene overexpression
dc.subjectheart muscle fibrosis
dc.subjectheart ventricle hypertrophy
dc.subjecthigh salt diet
dc.subjectimmunocompetent cell
dc.subjectimmunomodulation
dc.subjectin vitro study
dc.subjectinflammation
dc.subjectkidney disease
dc.subjectkidney fibrosis
dc.subjectkidney hypertrophy
dc.subjectmale
dc.subjectmouse
dc.subjectnephrectomy
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjecttarget organ
dc.subjectTh17 cell
dc.subjectvascular fibrosis
dc.subjectanimal
dc.subjectC57BL mouse
dc.subjectcardiomegaly
dc.subjectcardiovascular system
dc.subjectcoculture
dc.subjectcytology
dc.subjectdendritic cell
dc.subjectfibrosis
dc.subjectgenetics
dc.subjecthyperaldosteronism
dc.subjectkidney
dc.subjectknockout mouse
dc.subjectlymphocyte activation
dc.subjectmetabolism
dc.subjectsalt intake
dc.subjectT lymphocyte
dc.subjectAldosterone
dc.subjectAnimals
dc.subjectCardiomegaly
dc.subjectCardiovascular System
dc.subjectCD11 Antigens
dc.subjectCoculture Techniques
dc.subjectDendritic Cells
dc.subjectFemale
dc.subjectFibrosis
dc.subjectHyperaldosteronism
dc.subjectInflammation
dc.subjectInterleukin-23 Subunit p19
dc.subjectKidney
dc.subjectLipocalin-2
dc.subjectLymphocyte Activation
dc.subjectMale
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectNatriuretic Peptide, Brain
dc.subjectReceptors, Mineralocorticoid
dc.subjectSodium Chloride, Dietary
dc.subjectT-Lymphocytes
dc.titleDendritic cells are crucial for cardiovascular remodeling and modulate neutrophil gelatinase-associated lipocalin expression upon mineralocorticoid receptor activation
dc.typeArticle


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