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The Proinflammatory Phenotype of Senescent Cells: The p53‐Mediated ICAM‐1 Expression
Author(s) -
KLETSAS DIMITRIS,
PRATSINIS HARRIS,
MARIATOS GIORGOS,
ZACHARATOS PANAYOTIS,
GORGOULIS VASSILIS G.
Publication year - 2004
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1297.056
Subject(s) - proinflammatory cytokine , phenotype , microbiology and biotechnology , icam 1 , nfkb1 , suppressor , biology , inflammation , cell adhesion molecule , function (biology) , intercellular adhesion molecule 1 , cancer research , immunology , transcription factor , genetics , gene
A bstract : 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‐kappaB (NF‐κB) signaling cascade is crucial in ICAM‐1 activation, we have shown that p53 directly activates the expression of ICAM‐1 in an NF‐kB‐independent manner. This may link p53 to ICAM‐1 function and consequently to the aging process and to various age‐related pathologies.