2018
DOI: 10.18632/aging.101389
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Abstract: Little is known on how well senescence markers in vitro and in situ correlate within individual donors. We studied correlations between the same and different in vitro markers. Furthermore, we tested correlations between in vitro markers with in situ p16INK4a positivity.From 100 donors (20-91 years), cultured dermal fibroblasts were assessed for reactive oxygen species (ROS), telomere-associated foci (TAF), p16INK4a and senescence-associated β-gal (SAβ-gal), with/ without 0.6 µM rotenone for 3 days (short-term… Show more

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Cited by 15 publications
(7 citation statements)
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References 37 publications
(43 reference statements)
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“…Loss of lamin B1 protein was suggested to be a promising biomarker for senescence but its mRNA levels failed to distinguish senescence vs quiescent fibroblasts [120]. Several groups came up with various senescence-associated markers such as γ-H2A-X and 53BP1 foci [121], activated ataxia-telangiectasia mutated (ATM) kinase [122], telomere-associated DNA damage foci (TAF) [116,123,124,125], and a histone variant H2A.J [126]. Most of them were either employed individually or in combination, but the identification of a unique senescent cell-specific marker remains unsolved [127].…”
Section: Discussionmentioning
confidence: 99%
“…Loss of lamin B1 protein was suggested to be a promising biomarker for senescence but its mRNA levels failed to distinguish senescence vs quiescent fibroblasts [120]. Several groups came up with various senescence-associated markers such as γ-H2A-X and 53BP1 foci [121], activated ataxia-telangiectasia mutated (ATM) kinase [122], telomere-associated DNA damage foci (TAF) [116,123,124,125], and a histone variant H2A.J [126]. Most of them were either employed individually or in combination, but the identification of a unique senescent cell-specific marker remains unsolved [127].…”
Section: Discussionmentioning
confidence: 99%
“…Persistent DNA damage is a critical trigger of cellular senescence and can be identified by the presence of γ-H2A-X and 53BP1 foci ( D’Adda Di Fagagna et al, 2003 ) and activated ataxia-telangiectasia mutated (ATM) kinase ( Zou, 2007 ). However, while DNA damage per se , is not a marker for cellular senescence, the occurrence of telomere-associated DNA damage foci (TAF) has been used to detect senescent cells and quantify tissue aging ( Herbig et al, 2006 ; Jeyapalan et al, 2007 ; Hewitt et al, 2012 ; Waaijer et al, 2018 ). Replicative senescent baboon skin fibroblasts and skin biopsies from aged baboons displayed high incidence of TAF as indicated by co-localization of 53BP1 and γ-H2A-X on telomeric DNA ( Herbig et al, 2006 ; Jeyapalan et al, 2007 ).…”
Section: Senescence Biomarkersmentioning
confidence: 99%
“…Persistent ROS-induced DNA damage drives cellular senescence and can be identified by markers for DNA double-strand breaks, such as γH2AX, that are co-localized with DNA damage checkpoint factors including p53-binding protein 1 (53BP1), mediator of DNA damage checkpoint protein 1, and Nijmegen breakage syndrome 1 [ 33 ]. In addition, the occurrence of telomere-associated DNA damage foci (TAF) has been used to detect senescent cells and quantify tissue aging in situ [ 34 , 35 ]. Replicative senescent baboon skin fibroblasts and skin tissues from aged baboons revealed increased TAF as indicated by co-localization of 53BP1 and γH2AX on telomeric DNA [ 16 , 36 ].…”
Section: Fibroblast Senescencementioning
confidence: 99%