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- W3124268951 abstract "Pro-inflammatory M1 macrophage polarization is associated with microbicidal and antitumor responses. We recently described APOBEC3A-mediated cytosine-to-uracil (C > U) RNA editing during M1 polarization. However, the functional significance of this editing is unknown. Here we find that APOBEC3A-mediated cellular RNA editing can also be induced by influenza or Maraba virus infections in normal human macrophages, and by interferons in tumor-associated macrophages. Gene knockdown and RNA_Seq analyses show that APOBEC3A mediates C>U RNA editing of 209 exonic/UTR sites in 203 genes during M1 polarization. The highest level of nonsynonymous RNA editing alters a highly-conserved amino acid in THOC5, which encodes a nuclear mRNA export protein implicated in M-CSF-driven macrophage differentiation. Knockdown of APOBEC3A reduces IL6, IL23A and IL12B gene expression, CD86 surface protein expression, and TNF-α, IL-1β and IL-6 cytokine secretion, and increases glycolysis. These results show a key role of APOBEC3A cytidine deaminase in transcriptomic and functional polarization of M1 macrophages." @default.
- W3124268951 created "2021-02-01" @default.
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- W3124268951 date "2021-01-22" @default.
- W3124268951 modified "2023-10-10" @default.
- W3124268951 title "RNA editing enzyme APOBEC3A promotes pro-inflammatory M1 macrophage polarization" @default.
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- W3124268951 doi "https://doi.org/10.1038/s42003-020-01620-x" @default.
- W3124268951 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7822933" @default.
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