Diminished Reactive Hematopoiesis and Cardiac Inflammation in a Mouse Model of Recurrent Myocardial Infarction.
bone marrow
emergency hematopoiesis
immune memory
inflammation
recurrent myocardial infarction
Journal
Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365
Informations de publication
Date de publication:
03 03 2020
03 03 2020
Historique:
received:
22
06
2019
revised:
02
12
2019
accepted:
16
12
2019
entrez:
5
3
2020
pubmed:
5
3
2020
medline:
15
12
2020
Statut:
ppublish
Résumé
Recurrent myocardial infarction (MI) is common in patients with coronary artery disease and is associated with high mortality. Long-term reprogramming of myeloid progenitors occurs in response to inflammatory stimuli and alters the organism's response to secondary inflammatory challenges. This study examined the effect of recurrent MI on bone marrow response and cardiac inflammation. The investigators developed a surgical mouse model in which 2 subsequent MIs affected different left ventricular regions in the same mouse. Recurrent MI was induced by ligating the left circumflex artery followed by the left anterior descending coronary artery branch. The study characterized the resulting ischemia by whole-heart fluorescent coronary angiography after optical organ clearing and by cardiac magnetic resonance imaging. A first MI-induced bone marrow "memory" via a circulating signal, reducing hematopoietic maintenance factor expression in bone marrow macrophages. This dampened the organism's reaction to subsequent events. Despite a similar extent of injury according to troponin levels, recurrent MI caused reduced emergency hematopoiesis and less leukocytosis than a first MI. Consequently, fewer leukocytes migrated to the ischemic myocardium. The hematopoietic response to lipopolysaccharide was also mitigated after a previous MI. The increase of white blood count in 28 patients was lower after recurrent MI compared with their first MI. The data suggested that hematopoietic and innate immune responses are shaped by a preceding MI.
Sections du résumé
BACKGROUND
Recurrent myocardial infarction (MI) is common in patients with coronary artery disease and is associated with high mortality. Long-term reprogramming of myeloid progenitors occurs in response to inflammatory stimuli and alters the organism's response to secondary inflammatory challenges.
OBJECTIVES
This study examined the effect of recurrent MI on bone marrow response and cardiac inflammation.
METHODS
The investigators developed a surgical mouse model in which 2 subsequent MIs affected different left ventricular regions in the same mouse. Recurrent MI was induced by ligating the left circumflex artery followed by the left anterior descending coronary artery branch. The study characterized the resulting ischemia by whole-heart fluorescent coronary angiography after optical organ clearing and by cardiac magnetic resonance imaging.
RESULTS
A first MI-induced bone marrow "memory" via a circulating signal, reducing hematopoietic maintenance factor expression in bone marrow macrophages. This dampened the organism's reaction to subsequent events. Despite a similar extent of injury according to troponin levels, recurrent MI caused reduced emergency hematopoiesis and less leukocytosis than a first MI. Consequently, fewer leukocytes migrated to the ischemic myocardium. The hematopoietic response to lipopolysaccharide was also mitigated after a previous MI. The increase of white blood count in 28 patients was lower after recurrent MI compared with their first MI.
CONCLUSIONS
The data suggested that hematopoietic and innate immune responses are shaped by a preceding MI.
Identifiants
pubmed: 32130926
pii: S0735-1097(20)30165-0
doi: 10.1016/j.jacc.2019.12.056
pmc: PMC7254576
mid: NIHMS1569273
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
901-915Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL125428
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL076136
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL131478
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL142494
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL131495
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL139598
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Informations de copyright
Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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