Iron Regulator Hepcidin Impairs Macrophage-Dependent Cardiac Repair After Injury.
Animals
Animals, Newborn
Atrial Remodeling
/ physiology
Bone Marrow Cells
/ cytology
Heart
/ physiology
Hepcidins
/ genetics
Interleukin-13
/ metabolism
Interleukin-4
/ metabolism
Macrophages
/ cytology
Mesenchymal Stem Cell Transplantation
Mesenchymal Stem Cells
/ cytology
Mice
Mice, Inbred C57BL
Mice, Transgenic
Myocardial Infarction
/ pathology
Myocytes, Cardiac
/ cytology
Regeneration
Ventricular Remodeling
/ physiology
inflammation
macrophage
myocardial infarction
regeneration
Journal
Circulation
ISSN: 1524-4539
Titre abrégé: Circulation
Pays: United States
ID NLM: 0147763
Informations de publication
Date de publication:
19 03 2019
19 03 2019
Historique:
pubmed:
28
12
2018
medline:
31
12
2019
entrez:
28
12
2018
Statut:
ppublish
Résumé
Defective systemic and local iron metabolism correlates with cardiac disorders. Hepcidin, a master iron sensor, actively tunes iron trafficking. We hypothesized that hepcidin could play a key role to locally regulate cardiac homeostasis after acute myocardial infarction. Cardiac repair was analyzed in mice harboring specific cardiomyocyte or myeloid cell deficiency of hepcidin and challenged with acute myocardial infarction. We found that the expression of hepcidin was elevated after acute myocardial infarction and the specific deletion of hepcidin in cardiomyocytes failed to improve cardiac repair and function. However, transplantation of bone marrow-derived cells from hepcidin-deficient mice ( Hamp Hepcidin refrains macrophage-induced cardiac repair and regeneration through modulation of IL-4/IL-13 pathways.
Sections du résumé
BACKGROUND
Defective systemic and local iron metabolism correlates with cardiac disorders. Hepcidin, a master iron sensor, actively tunes iron trafficking. We hypothesized that hepcidin could play a key role to locally regulate cardiac homeostasis after acute myocardial infarction.
METHODS
Cardiac repair was analyzed in mice harboring specific cardiomyocyte or myeloid cell deficiency of hepcidin and challenged with acute myocardial infarction.
RESULTS
We found that the expression of hepcidin was elevated after acute myocardial infarction and the specific deletion of hepcidin in cardiomyocytes failed to improve cardiac repair and function. However, transplantation of bone marrow-derived cells from hepcidin-deficient mice ( Hamp
CONCLUSIONS
Hepcidin refrains macrophage-induced cardiac repair and regeneration through modulation of IL-4/IL-13 pathways.
Identifiants
pubmed: 30586758
doi: 10.1161/CIRCULATIONAHA.118.034545
doi:
Substances chimiques
Hepcidins
0
Interleukin-13
0
Interleukin-4
207137-56-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM