TNF-α-mediated microRNA-136 induces differentiation of myeloid cells by targeting NFIA

Journal of Leukocyte Biology
Shiyue MeiRongcun Yang

Abstract

Immune cell-lineage specification and function are influenced by progenitor origin and environmental factors. The mechanism of differentiation of immune cells, such as neutrophils, monocytes, and myeloid-derived suppressor cells, in inflammatory environments has not been elucidated completely. In this study, we have identified human microRNA-136 as a positive regulator of the differentiation of granulocytes and monocytes. Ectopic microRNA-136 induced cells to express higher levels of CD11b, CD14, and C/EBPε, secrete more cytokines, and synthesize higher levels of reactive oxygen species and H2O2. microRNA-136 was shown to target and degrade multiple differentiation-associated molecules, such as the transcription factor NFIA, which induced the release of another microRNA, microRNA-223, with the ability to promote CD11b expression. Furthermore, microRNA-136 expression was remarkably increased by TNF-α, which activated NF-κB to bind to the DNA-promoter region controlling microRNA-136 expression. Additionally, TNF-α may alter NFIA expression through its modulation of microRNA-136 expression. Thus, TNF-α-mediated microRNA-136 may play a critical role in the generation and differentiation of inflammatory immune cells.

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Citations

May 5, 2017·International Reviews of Immunology·S Manoj Kumar Kingsley, B Vishnu Bhat
Apr 23, 2016·Inflammatory Bowel Diseases·Dalin LiStephan R Targan
Mar 30, 2020·The Journal of Immunology : Official Journal of the American Association of Immunologists·Meihua ZhangJi Ming Wang
Aug 28, 2021·Biochimica Et Biophysica Acta. Molecular Basis of Disease·Maaike G J M van BergenBert A van der Reijden

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