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Coexpression of the genes for platelet-derived growth factor B-chain receptor and macrophage colony-stimulating

P Pantazis1, S Kharbanda, A S Goustin

  • 1Stehlin Foundation for Cancer Research, St. Joseph Hospital Cancer Research Laboratory, Houston, TX 77003.

Insights

Human myeloid cells that produce platelet-derived growth factor (PDGF) also express its receptor (PDGF-BR). This study identifies both full-length and truncated PDGF-BR mRNA and protein in differentiated myeloid cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Hematology

Background:

  • Human myeloid cells synthesize platelet-derived growth factor (PDGF).
  • PDGF receptors (PDGF-BR) were previously unidentified in human myeloid cells.
  • The role of autocrine PDGF signaling in myeloid cells remains unclear.

Purpose of the Study:

  • To investigate the expression of PDGF receptors in human myeloid cells.
  • To characterize the molecular forms of PDGF-BR in differentiated myeloid cells.
  • To examine the coexpression of PDGF-BR and macrophage colony-stimulating factor 1 receptor (M-CSFR) genes.

Main Methods:

  • Treatment of myeloid cells with phorbol ester to induce monocytic differentiation.
  • Detection of PDGF-BR mRNA using Northern blot analysis.
  • Immunofluorescence and immunoprecipitation assays to identify PDGF-BR protein.
  • Analysis of gene coexpression using molecular techniques.

Main Results:

  • Phorbol ester-differentiated myeloid cells express both 5.5-kb and 4.6-kb PDGF-BR mRNA.
  • PDGF-BR protein was detected in differentiated myeloid cells via immunofluorescence and immunoprecipitation.
  • PDGF-BR molecules of 37 kDa to 130 kDa were identified in cell lysates.
  • Tandemly linked genes for PDGF-BR and M-CSFR are coexpressed in these cells.

Conclusions:

  • Human myeloid cells differentiated along the monocytic lineage express PDGF-BR.
  • This expression includes both full-length and truncated receptor forms.
  • Coexpression of PDGF-BR and M-CSFR genes is demonstrated in these myeloid cells, suggesting novel autocrine/paracrine signaling pathways.

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