The proinflammatory phenotype of senescent cells: the p53-mediated ICAM-1 expression

Ann N Y Acad Sci. 2004 Jun;1019:330-2. doi: 10.1196/annals.1297.056.

Abstract

Senescent cells are characterized by the activation of the tumor suppressor protein p53 and consequently their inability to proliferate. However, their phenotype is not restricted to the exhaustion of their replicative potential, as they also exhibit a proinflammatory phenotype, which could possibly contribute to the aging process. Intercellular adhesion molecule-1 (ICAM-1) is one of the molecules involved in inflammatory response that is overexpressed in senescent cells and aged tissues. Although the role of the nuclear factor-kappa B (NF-kappa B) signaling cascade is crucial in ICAM-1 activation, we have shown that p53 directly activates the expression of ICAM-1 in an NF-kappa B-independent manner. This may link p53 to ICAM-1 function and consequently to the aging process and to various age-related pathologies.

Publication types

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

MeSH terms

  • Cell Division
  • Cells, Cultured
  • Cellular Senescence*
  • Humans
  • Inflammation*
  • Intercellular Adhesion Molecule-1 / biosynthesis*
  • NF-kappa B / metabolism
  • Phenotype
  • Signal Transduction
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • NF-kappa B
  • Tumor Suppressor Protein p53
  • Intercellular Adhesion Molecule-1