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- Publisher Website: 10.1097/HJH.0000000000002067
- Scopus: eid_2-s2.0-85067269649
- PMID: 31033725
- WOS: WOS:000480761700022
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Article: Dendritic cells are crucial for cardiovascular remodeling and modulate neutrophil gelatinase-associated lipocalin expression upon mineralocorticoid receptor activation
Title | Dendritic cells are crucial for cardiovascular remodeling and modulate neutrophil gelatinase-associated lipocalin expression upon mineralocorticoid receptor activation |
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Authors | |
Keywords | neutrophil gelatinase-associated lipocalin inflammation cardiovascular fibrosis mineralocorticoid receptor dendritic cells |
Issue Date | 2019 |
Citation | Journal of Hypertension, 2019, v. 37, n. 7, p. 1482-1492 How to Cite? |
Abstract | © 2019 Wolters Kluwer Health, Inc. All rights reserved. Background: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. |
Persistent Identifier | http://hdl.handle.net/10722/292115 |
ISSN | 2023 Impact Factor: 3.3 2023 SCImago Journal Rankings: 1.134 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Araos, Patricio | - |
dc.contributor.author | Prado, Carolina | - |
dc.contributor.author | Lozano, Mauricio | - |
dc.contributor.author | Figueroa, Stefanny | - |
dc.contributor.author | Espinoza, Alexandra | - |
dc.contributor.author | Berger, Thorsten | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Jaisser, Frédéric | - |
dc.contributor.author | Pacheco, Rodrigo | - |
dc.contributor.author | Michea, Luis | - |
dc.contributor.author | Amador, Cristián A. | - |
dc.date.accessioned | 2020-11-17T14:55:48Z | - |
dc.date.available | 2020-11-17T14:55:48Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Journal of Hypertension, 2019, v. 37, n. 7, p. 1482-1492 | - |
dc.identifier.issn | 0263-6352 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292115 | - |
dc.description.abstract | © 2019 Wolters Kluwer Health, Inc. All rights reserved. Background: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. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Hypertension | - |
dc.subject | neutrophil gelatinase-associated lipocalin | - |
dc.subject | inflammation | - |
dc.subject | cardiovascular fibrosis | - |
dc.subject | mineralocorticoid receptor | - |
dc.subject | dendritic cells | - |
dc.title | Dendritic cells are crucial for cardiovascular remodeling and modulate neutrophil gelatinase-associated lipocalin expression upon mineralocorticoid receptor activation | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1097/HJH.0000000000002067 | - |
dc.identifier.pmid | 31033725 | - |
dc.identifier.scopus | eid_2-s2.0-85067269649 | - |
dc.identifier.volume | 37 | - |
dc.identifier.issue | 7 | - |
dc.identifier.spage | 1482 | - |
dc.identifier.epage | 1492 | - |
dc.identifier.eissn | 1473-5598 | - |
dc.identifier.isi | WOS:000480761700022 | - |
dc.identifier.issnl | 0263-6352 | - |