Journal
CELLULAR IMMUNOLOGY
Volume 365, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2021.104377
Keywords
Leukemic microenvironment; Macrophage; MicroRNA profiling; MiR-451a
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Funding
- National Natural Science Foundation of China (NSFC) [81770183, 81970155]
- CAMS Innovation Fund for Medical Sciences (CIFMS) [2016-I2M-2-006, 2017-I2M-1-015]
- State Key Laboratory of Experimental Hematology Research Grant [Z20-06]
- New Century Excellent Talents in University [NCET-08-0329]
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The study revealed the heterogeneity of miRNA expression profiles in LAMs, and showed that overexpression of miR-451a can alter the morphology of macrophages, enhance their phagocytic ability, and promote the expression of differentiation marker CD11b. Moreover, miR-451a was found to increase the proliferation capacity of both M1- and M2-polarized macrophages.
Leukemia associated macrophages (LAMs), which are different from tumor-associated macrophages as well as classical M1 and M2 macrophages, are specifically activated by leukemic microenvironment. We have reported the heterogeneity of gene expression profiles in LAMs. However, the expression profiles of microRNA (miRNA) in LAMs and their regulatory mechanisms have not been established. Here, the expression profiles of miRNA in LAMs from bone marrow and spleen of acute myeloid leukemia mice were analyzed. Then, the effects of miR451a, which was upregulated in LAMs, on macrophages were studied by transfecting miRNA mimic to peritoneal macrophages. The results showed that overexpression of miR-451a altered the morphology, enhanced the phagocytic ability of macrophages, and promotes the expression of differentiation marker CD11b in macrophages. Furthermore, miR-451a increased the proliferation capacity of both M1- and M2-polarized macrophages, but not M0 macrophages. Moreover, miR-451a further enhanced the expression of iNOS upon M1 activation. Therefore, our results reveal the miRNA expression profiles in LAMs, and broaden the knowledge about miRNA regulation in macrophages.
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