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Statements

Subject Item
n2:RIV%2F00209805%3A_____%2F13%3A%230000432%21RIV14-GA0-00209805
rdf:type
skos:Concept n12:Vysledek
rdfs:seeAlso
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859419/pdf/JCI70355.pdf
dcterms:description
Cellular senescence contributes to aging and decline in tissue function. p53 isoform switching regulates replicative senescence in cultured fibroblasts and is associated with tumor progression. Here, we found that the endogenous p53 isoforms Δ133p53 and p53β are physiological regulators of proliferation and senescence in human T lymphocytes in vivo. Peripheral blood CD8+ T lymphocytes collected from healthy donors displayed an age-dependent accumulation of senescent cells (CD28–CD57+) with decreased Δ133p53 and increased p53β expression. Human lung tumor-associated CD8+ T lymphocytes also harbored senescent cells. Cultured CD8+ blood T lymphocytes underwent replicative senescence that was associated with loss of CD28 and Δ133p53 protein. In poorly proliferative, Δ133p53-low CD8+CD28– cells, reconstituted expression of either Δ133p53 or CD28 upregulated endogenous expression of each other, which restored cell proliferation, extended replicative lifespan and rescued senescence phenotypes. Conversely, Δ133p53 knockdown or p53β overexpression in CD8+CD28+ cells inhibited cell proliferation and induced senescence. This study establishes a role for Δ133p53 and p53β in regulation of cellular proliferation and senescence in vivo. Furthermore, Δ133p53-induced restoration of cellular replicative potential may lead to a new therapeutic paradigm for treating immunosenescence disorders, including those associated with aging, cancer, autoimmune diseases, and HIV infection. Cellular senescence contributes to aging and decline in tissue function. p53 isoform switching regulates replicative senescence in cultured fibroblasts and is associated with tumor progression. Here, we found that the endogenous p53 isoforms Δ133p53 and p53β are physiological regulators of proliferation and senescence in human T lymphocytes in vivo. Peripheral blood CD8+ T lymphocytes collected from healthy donors displayed an age-dependent accumulation of senescent cells (CD28–CD57+) with decreased Δ133p53 and increased p53β expression. Human lung tumor-associated CD8+ T lymphocytes also harbored senescent cells. Cultured CD8+ blood T lymphocytes underwent replicative senescence that was associated with loss of CD28 and Δ133p53 protein. In poorly proliferative, Δ133p53-low CD8+CD28– cells, reconstituted expression of either Δ133p53 or CD28 upregulated endogenous expression of each other, which restored cell proliferation, extended replicative lifespan and rescued senescence phenotypes. Conversely, Δ133p53 knockdown or p53β overexpression in CD8+CD28+ cells inhibited cell proliferation and induced senescence. This study establishes a role for Δ133p53 and p53β in regulation of cellular proliferation and senescence in vivo. Furthermore, Δ133p53-induced restoration of cellular replicative potential may lead to a new therapeutic paradigm for treating immunosenescence disorders, including those associated with aging, cancer, autoimmune diseases, and HIV infection.
dcterms:title
p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes
skos:prefLabel
p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes
skos:notation
RIV/00209805:_____/13:#0000432!RIV14-GA0-00209805
n12:predkladatel
n17:ico%3A00209805
n4:aktivita
n13:P
n4:aktivity
P(ED2.1.00/03.0101), P(GAP301/11/1678), P(GBP206/12/G151)
n4:cisloPeriodika
12
n4:dodaniDat
n15:2014
n4:domaciTvurceVysledku
n18:9637419
n4:druhVysledku
n10:J
n4:duvernostUdaju
n8:S
n4:entitaPredkladatele
n5:predkladatel
n4:idSjednocenehoVysledku
101111
n4:idVysledku
RIV/00209805:_____/13:#0000432
n4:jazykVysledku
n16:eng
n4:klicovaSlova
cellular senescence; human cells; therapeutic opportunities; shortened telomeres; secretory phenotype; HIV-infection; life-span; expression; cancer; memory
n4:klicoveSlovo
n7:cellular%20senescence n7:secretory%20phenotype n7:HIV-infection n7:life-span n7:shortened%20telomeres n7:cancer n7:therapeutic%20opportunities n7:expression n7:human%20cells n7:memory
n4:kodStatuVydavatele
US - Spojené státy americké
n4:kontrolniKodProRIV
[25913377124A]
n4:nazevZdroje
The Journal of Clinical Investigation
n4:obor
n20:EB
n4:pocetDomacichTvurcuVysledku
1
n4:pocetTvurcuVysledku
12
n4:projekt
n11:GAP301%2F11%2F1678 n11:ED2.1.00%2F03.0101 n11:GBP206%2F12%2FG151
n4:rokUplatneniVysledku
n15:2013
n4:svazekPeriodika
123
n4:tvurceVysledku
Vojtěšek, Bořivoj
n4:wos
000327826100029
s:issn
0021-9738
s:numberOfPages
11
n3:doi
10.1172/JCI70355