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

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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

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Shiyue Mei1, Yu Liu1, Xue Wu1

  • 1*Department of Immunology, School of Medicine, State Key Laboratory of Medicinal Chemical Biology, and Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, Tianjin, P. R. China.

Journal of Leukocyte Biology
|September 3, 2015
PubMed

Insights

Human microRNA-136 promotes granulocyte and monocyte differentiation by regulating key molecules. Tumor Necrosis Factor-alpha enhances microRNA-136, impacting inflammatory immune cell generation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Immune cell differentiation is influenced by progenitor origin and environmental cues.
  • Mechanisms governing immune cell differentiation in inflammation, including neutrophils, monocytes, and myeloid-derived suppressor cells, require further elucidation.

Purpose of the Study:

  • To identify regulators of immune cell differentiation in inflammatory environments.
  • To investigate the role of human microRNA-136 (miRNA-136) in granulocyte and monocyte differentiation.

Main Methods:

  • Ectopic expression of miRNA-136 in cells.
  • Analysis of cell surface marker expression (CD11b, CD14), cytokine secretion, and reactive oxygen species production.
  • Investigation of miRNA-136 targeting of differentiation-associated molecules, including transcription factor NFIA.
  • Assessment of miRNA-223 induction and its effect on CD11b expression.
  • Examination of TNF-α-induced miRNA-136 expression via NF-κB activation and its impact on NFIA.

Main Results:

  • Ectopic miRNA-136 increased CD11b, CD14, and C/EBPε expression, cytokine secretion, and reactive oxygen species/H2O2 synthesis.
  • miRNA-136 targeted and degraded NFIA, leading to the release of miRNA-223, which promotes CD11b expression.
  • Tumor Necrosis Factor-alpha (TNF-α) significantly upregulated miRNA-136 expression by activating NF-κB.
  • TNF-α may modulate NFIA expression through its regulation of miRNA-136.

Conclusions:

  • Human miRNA-136 acts as a positive regulator of granulocyte and monocyte differentiation.
  • The TNF-α/NF-κB/miRNA-136 axis plays a crucial role in the generation and differentiation of inflammatory immune cells.
Keywords:
hematopoieticinflammatory environmentneutrophil

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