Effect of mitogenic stimulation and DNA methylation on human T cell DNA methyltransferase expression and activity

J Immunol. 1997 Aug 1;159(3):1303-9.

Abstract

DNA methylation, a mechanism modifying gene expression, is mediated in part by the enzyme DNA methyltransferase. Reduced levels of T cell DNA methyltransferase have been observed in lupus-like diseases, and increased levels have been reported in malignancies. Little is known concerning the regulation of human DNA methyltransferase. In this report we demonstrate that mitogenic T cell stimulation causes an increase in DNA methyltransferase mRNA and enzyme activity. We also show that pharmacologic inhibition of T cell DNA methylation causes an increase in the rate of DNA methyltransferase mRNA transcription and a corresponding increase in mRNA levels and enzyme activity. This suggests that DNA methyltransferase is itself regulated in part by DNA methylation status, possibly representing a feedback mechanism. DNA methylation inhibition also resulted in an increase in Ha-ras and c-jun mRNA levels, overexpression of which increases DNA methyltransferase in murine systems. These results thus identify two mechanisms regulating levels of human T cell DNA methyltransferase and raise the possibility that abnormalities in either could contribute to disorders associated with altered DNA methylation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Azacitidine / pharmacology
  • DNA Methylation / drug effects
  • DNA-Cytosine Methylases / antagonists & inhibitors
  • DNA-Cytosine Methylases / biosynthesis*
  • DNA-Cytosine Methylases / genetics
  • Enzyme Activation / drug effects
  • Humans
  • Jurkat Cells
  • Lymphocyte Activation / drug effects*
  • Male
  • Phytohemagglutinins / pharmacology*
  • Procainamide / pharmacology*
  • RNA, Messenger / drug effects
  • RNA, Messenger / genetics
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / enzymology*
  • T-Lymphocytes / immunology*
  • Transcription, Genetic / drug effects

Substances

  • Phytohemagglutinins
  • RNA, Messenger
  • DNA-Cytosine Methylases
  • Procainamide
  • Azacitidine