Effect of protein kinase C on T lymphocyte proliferation and apoptosis in acute idiopathic thrombocytopenic purpura

Acta Haematol. 2006;116(3):173-80. doi: 10.1159/000094677.

Abstract

Previous studies have shown that T lymphocyte proliferation and apoptosis are abnormal in idiopathic thrombocytopenic purpura (ITP) children; however, the underlying regulated mechanisms in signal transductions remain unknown. In this paper, we investigated the changes of protein kinase C (PKC) activity in peripheral blood T lymphocytes and the effect of PKC on the peripheral blood T lymphocyte proliferation and apoptosis in ITP children. We demonstrated that T lymphocytes from ITP children were more susceptible to the activator (phorbol myristate acetate) and the inhibitor (H-7) of PKC. In ITP children, phorbol myristate acetate and H-7 dramatically affected T lymphocyte proliferation and apoptosis, but altered little in healthy children. Compared with healthy children, PKC activity was significantly enhanced in ITP children, increasing the expressions of Fas ligand on CD3+, CD4+ and CD8+ T cells, indicating positive correlations between PKC activity and the expressions of Fas ligand on T cells, while the relations between PKC activity and platelet count showed negative correlations. Taken together, our findings suggest that PKC signal transductions may participate in the procedure of T lymphocyte proliferation and apoptosis in ITP children. PKC activation may enhance T lymphocyte activity, suppress T cell apoptosis, and be involved in thrombocyte damage, which can be related to the immunity pathogenesis of ITP.

MeSH terms

  • Acute Disease
  • Adolescent
  • Apoptosis / drug effects*
  • Cell Proliferation / drug effects*
  • Child
  • Child, Preschool
  • DNA / analysis
  • Electrophoresis, Agar Gel
  • Fas Ligand Protein
  • Female
  • Humans
  • Infant
  • Male
  • Membrane Glycoproteins / metabolism
  • Protein Kinase C / blood*
  • Purpura, Thrombocytopenic, Idiopathic / enzymology*
  • Signal Transduction / physiology
  • T-Lymphocytes / cytology*
  • Tumor Necrosis Factors / metabolism

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • Tumor Necrosis Factors
  • DNA
  • Protein Kinase C