Rho GTPase expression in human myeloid cells

PLoS One. 2012;7(8):e42563. doi: 10.1371/journal.pone.0042563. Epub 2012 Aug 16.

Abstract

Myeloid cells are critical for innate immunity and the initiation of adaptive immunity. Strict regulation of the adhesive and migratory behavior is essential for proper functioning of these cells. Rho GTPases are important regulators of adhesion and migration; however, it is unknown which Rho GTPases are expressed in different myeloid cells. Here, we use a qPCR-based approach to investigate Rho GTPase expression in myeloid cells.We found that the mRNAs encoding Cdc42, RhoQ, Rac1, Rac2, RhoA and RhoC are the most abundant. In addition, RhoG, RhoB, RhoF and RhoV are expressed at low levels or only in specific cell types. More differentiated cells along the monocyte-lineage display lower levels of Cdc42 and RhoV, while RhoC mRNA is more abundant. In addition, the Rho GTPase expression profile changes during dendritic cell maturation with Rac1 being upregulated and Rac2 downregulated. Finally, GM-CSF stimulation, during macrophage and osteoclast differentiation, leads to high expression of Rac2, while M-CSF induces high levels of RhoA, showing that these cytokines induce a distinct pattern. Our data uncover cell type specific modulation of the Rho GTPase expression profile in hematopoietic stem cells and in more differentiated cells of the myeloid lineage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD34 / immunology
  • Cell Differentiation
  • Cells, Cultured
  • Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology
  • Humans
  • Macrophage Colony-Stimulating Factor / pharmacology
  • Myeloid Cells / drug effects
  • Myeloid Cells / immunology
  • Myeloid Cells / metabolism*
  • rho GTP-Binding Proteins / metabolism*

Substances

  • Antigens, CD34
  • Macrophage Colony-Stimulating Factor
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • rho GTP-Binding Proteins

Grants and funding

This project was funded by Sanquin. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.