IL-4 inhibits cell cycle progression of human umbilical vein endothelial cells by affecting p53, p21(Waf1), cyclin D1, and cyclin E expression

Mol Cells. 2003 Aug 31;16(1):92-6.

Abstract

IL-4 is emerging as a candidate cytokine for the treatment of inflammatory and autoimmune diseases. We have reported that IL-4 has anti-angiogenic activity and inhibits the growth of human umbilical vein endothelial cells (HUVEC) in response to vascular endothelial growth factor (VEGF) or fibroblast growth factor-2 (FGF-2). Cell cycle analysis of this effect revealed that IL-4 arrests the growth of FGF-2-stimulated HUVEC in G0 + G1 phases. The absence of subdiploid cells showed that it did not induce apoptosis. Growth arrest was dose-dependent, but the percentage of G0 + G1 phase cells never exceeded 85%. An immunoblot analysis demonstrated that expression of p53 and p21(Waf1) was increased and that of cyclin D1 and cyclin E decreased by IL-4. These results show that IL-4 inhibits endothelial cell growth by altering the expression of cell cycle regulatory molecules.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle / physiology*
  • Cells, Cultured
  • Cyclin D1 / metabolism*
  • Cyclin E / metabolism*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / metabolism*
  • Endothelial Cells / cytology
  • Endothelial Cells / metabolism*
  • Fibroblast Growth Factor 2 / metabolism
  • Humans
  • Interleukin-4 / metabolism*
  • Tumor Suppressor Protein p53 / metabolism*
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • CDKN1A protein, human
  • Cyclin E
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Tumor Suppressor Protein p53
  • Vascular Endothelial Growth Factor A
  • Fibroblast Growth Factor 2
  • Cyclin D1
  • Interleukin-4