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Reactive oxygen species regulate M-CSF-induced monocyte/macrophage proliferation through SHP1 oxidation

Han Kyoung Choi1, Tae Hee Kim, Gil-Ja Jhon

  • 1Division of Life and Pharmaceutical Sciences, Center for Cell Signaling & Drug Discovery Research, Ewha Womans University, Seoul, Republic of Korea.

Cellular Signalling
|June 14, 2011
PubMed

Insights

Macrophage colony-stimulating factor (M-CSF) triggers reactive oxygen species (ROS) to drive monocyte/macrophage proliferation. This study reveals M-CSF-induced ROS activate SHP1 phosphatase, promoting proliferation via the PI3K/Akt pathway.

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Signaling

Background:

  • Macrophage colony-stimulating factor (M-CSF) stimulates monocyte/macrophage proliferation.
  • Reactive oxygen species (ROS) are involved in M-CSF-induced proliferation, but their regulatory mechanisms are unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which ROS modulate M-CSF signaling.
  • To identify key regulators of M-CSF-mediated proliferation in bone marrow monocyte/macrophage lineage cells (BMMs).

Main Methods:

  • Inhibition of ROS production using diphenylene iodonium (DPI).
  • Manipulation of SHP1 expression (overexpression and RNA interference) in BMMs.
  • Analysis of signaling pathways including c-Fms, Akt, ERK, p38, and JNK phosphorylation.
  • Assessment of cell proliferation and cyclin D1/D2 expression.

Main Results:

  • DPI treatment inhibited M-CSF-induced ROS production, proliferation, and phosphorylation of c-Fms and Akt, but not MAP kinases.
  • SHP1 dysregulation demonstrated its specific, redox-dependent regulation of PI3K/Akt signaling, independent of MAP kinases.
  • SHP1 regulates BMM proliferation through cyclins D1 and D2.

Conclusions:

  • M-CSF-mediated ROS generation leads to SHP1 oxidation.
  • Oxidized SHP1 promotes BMM proliferation via the PI3K/Akt signaling pathway.
  • SHP1 is a critical redox-sensitive regulator of M-CSF signaling in BMMs.

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