Claudio Vinegoni, Ph.D. | Diminished Reactive Hematopoiesis and Cardiac Inflammation in a Mouse Model of Recurrent Myocardial Infarction

J. Am. Coll. Cardiol.
Diminished Reactive Hematopoiesis and Cardiac Inflammation in a Mouse Model of Recurrent Myocardial Infarction

Cremer, S., Schloss, M. J., Vinegoni, C., Foy, B. H., Zhang, S., Rohde, D., Hulsmans, M., Feruglio, P. F., Schmidt, S., Wojtkiewicz, G., Higgins, J. M., Weissleder, R., Swirski, F. K., and Nahrendorf^#, M.

Journal of the American College of Cardiology 2020

ABS URL PMID DOI PMCID CITE HTML PDF

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 drculating 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 ML 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. (C) 2020 by the American College of Cardiology Foundation.
@article{2020-JAMCC, author= {Cremer, S. and Schloss, M. J. and Vinegoni, C. and Foy, B. H. and Zhang, S. and Rohde, D. and Hulsmans, M. and Feruglio, P. F. and Schmidt, S. and Wojtkiewicz, G. and Higgins, J. M. and Weissleder, R. and Swirski, F. K. and Nahrendorf<sup>#</sup>, M.}, title= {Diminished Reactive Hematopoiesis and Cardiac Inflammation in a Mouse Model of Recurrent Myocardial Infarction}, journal= {Journal of the American College of Cardiology}, alternatejournal = {J. Am. Coll. Cardiol.}, year = {2020}, volume = {75}, number = {8}, pages = {901-915}, issn = {0735-1097}, doi = {10.1016/j.jacc.2019.12.056}, pmcid = {PMC7254576}, pmid= {32130926} }
32130926

PMC7254576

10.1016/j.jacc.2019.12.056

Abstract

"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 drculating 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 ML 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. (C) 2020 by the American College of Cardiology Foundation."

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For attribution in academic contexts, please cite this work as:

Cremer, S., Schloss, M. J., Vinegoni, C., Foy, B. H., Zhang, S., Rohde, D., Hulsmans, M., Feruglio, P. F., Schmidt, S., Wojtkiewicz, G., Higgins, J. M., Weissleder, R., Swirski, F. K., & Nahrendorf^#, M. (2020). Diminished Reactive Hematopoiesis and Cardiac Inflammation in a Mouse Model of Recurrent Myocardial Infarction. Journal of the American College of Cardiology, 75(8), 901–915. https://doi.org/10.1016/j.jacc.2019.12.056