title: Stress-induced premature senescence or stress-induced senescence-like phenotype: one in vivo reality, two possible definitions?
abstract: No consensus exists so far on the definition of cellular senescence. The narrowest definition of senescence is irreversible growth arrest triggered by telomere shortening counting cell generations (definition 1). Other authors gave an enlarged functional definition encompassing any kind of irreversible arrest of proliferative cell types induced by damaging agents or cell cycle deregulations after overexpression of proto-oncogenes (definition 2). As stress increases, the proportion of cells in "stress-induced premature senescence-like phenotype" according to definition 1 or "stress-induced premature senescence," according to definition 2, should increase when a culture reaches growth arrest, and the proportion of cells that reached telomere-dependent replicative senescence due to the end-replication problem should decrease. Stress-induced premature senescence-like phenotype and telomere-dependent replicatively senescent cells share basic similarities such as irreversible growth arrest and resistance to apoptosis, which may appear through different pathways. Irreversible growth arrest after exposure to oxidative stress and generation of DNA damage could be as efficient in avoiding immortalisation as "telomere-dependent" replicative senescence. Probabilities are higher that the senescent cells (according to definition 2) appearing in vivo are in stress-induced premature senescence rather than in telomere-dependent replicative senescence. Examples are given suggesting these cells affect in vivo tissue (patho)physiology and aging.
authors.affiliation: University of Namur (FUNDP), Department of Biology, Research Unit of Cellular Biology (URBC), Namur, Belgium. olivier.toussaint@fundp.ac.be
authors.forename: Olivier
authors.initials: O
authors.lastname: Toussaint
authors.forename: Patrick
authors.initials: P
authors.lastname: Dumont
authors.forename: José
authors.initials: J
authors.lastname: Remacle
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Dierick
authors.forename: Thierry
authors.initials: T
authors.lastname: Pascal
authors.forename: Christophe
authors.initials: C
authors.lastname: Frippiat
authors.forename: Joao Pedro
authors.initials: JP
authors.lastname: Magalhaes
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Zdanov
authors.forename: Florence
authors.initials: F
authors.lastname: Chainiaux
mesh_terms: D000375:Aging; D000818:Animals; D002453:Cell Cycle; D002455:Cell Division; D002478:Cells, Cultured; D016922:Cellular Senescence; D015870:Gene Expression; D006801:Humans; D008962:Models, Theoretical; D018384:Oxidative Stress; D010641:Phenotype; D013312:Stress, Physiological / Q000378:metabolism / Q000473:pathology; D016615:Telomere / Q000737:chemistry; D009626:Terminology as Topic