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Epigenetic control of PRV-1 expression on neutrophils

Jaroslav Jelinek1, Jun Li, Zakar Mnjoyan

  • 1Department of Leukemia, University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.

Experimental Hematology
|November 3, 2007
PubMed

Insights

DNA methylation regulates Polycythemia rubra vera-1 (PRV-1) gene expression. Lower methylation correlates with increased PRV-1 in normal neutrophils and myeloproliferative disorders like PV and ET.

Area of Science:

  • Hematology
  • Molecular Biology
  • Epigenetics

Background:

  • Polycythemia rubra vera-1 (PRV-1) is a GPI-linked protein expressed on neutrophils.
  • PRV-1 expression increases in pregnancy, sepsis, and with G-CSF administration.
  • PRV-1 gene expression is elevated in polycythemia vera (PV) and essential thrombocythemia (ET).

Purpose of the Study:

  • To investigate the role of DNA methylation in regulating PRV-1 gene transcription and protein expression.
  • To determine if DNA methylation patterns differ in PRV-1 expressing versus non-expressing neutrophils.
  • To examine PRV-1 methylation in myeloproliferative neoplasms.

Main Methods:

  • Compared PRV-1 gene methylation and mRNA expression in normal PRV-1 positive and negative neutrophils.
  • Studied PRV-1 methylation and mRNA in patients with Philadelphia chromosome-negative myeloproliferative disorders.
  • Utilized an in vitro model of DNA demethylation using KG1 and KG1a cells.

Main Results:

  • Methylation of CpG dinucleotides near the PRV-1 initiation codon was inversely related to PRV-1 expression in normal neutrophils.
  • Overexpression of PRV-1 in PV and ET was associated with decreased PRV-1 gene methylation.
  • PRV-1 methylation inversely correlated with the JAK2(V617F) mutation in PV and ET patients.
  • In vitro DNA demethylation decreased PRV-1 methylation and increased its mRNA levels.

Conclusions:

  • DNA methylation is a key regulator of PRV-1 expression.
  • This regulation occurs under both physiological and pathological conditions.
  • Findings suggest a role for epigenetic mechanisms in myeloproliferative disorders.
Abstract

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