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Myocardial infarction induces bone marrow megakaryocyte proliferation, maturation and platelet production

Fu, Wenwen, Wang, Jichun, Jiang, Hong, Hu, Xiaorong
Biochemical and biophysical research communications 2019 v.510 no.3 pp. 456-461
animal models, atherosclerosis, blood platelets, bone marrow, coronary vessels, flow cytometry, fluorescent antibody technique, homeostasis, myocardial infarction, spleen, staining, therapeutics
Platelet, apart from its classic role of homeostasis, serves also as a crucial immune cell component that contributes to the aggravation of atherosclerosis. It has been reported that myocardial infarction (MI) triggers leukocytosis in the bone marrow and spleen, which accelerates post-MI atherosclerosis. However, it remains unclear whether thrombopoiesis is also enhanced after MI. Here, using flow cytometry and bone marrow whole-mount immunofluorescence staining combined with three-dimensional (3D) reconstruction, we for the first time demonstrated an enhanced thrombopoiesis and megakaryopoiesis in a mouse model of coronary artery ligation as a mimic of MI. We showed that MI leads to increasing number of peripheral platelets, as well as elevating number and larger size of bone marrow MKs. We also observed more proplatelets and fragmented MKs, and a closer spatial distribution of MK populations to the bone marrow vascular niche after MI. This study provides direct evidence that MI induces bone marrow megakaryocyte proliferation, maturation and platelet production. It opens a new scope that targeting platelet production might become a novel therapeutic approach for attenuating post-MI atherosclerosis.