p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F13%3A%230000432" target="_blank" >RIV/00209805:_____/13:#0000432 - isvavai.cz</a>

Výsledek na webu

<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859419/pdf/JCI70355.pdf" target="_blank" >http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859419/pdf/JCI70355.pdf</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1172/JCI70355" target="_blank" >10.1172/JCI70355</a>

Jazyk výsledku

angličtina

Název v původním jazyce

p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes

Popis výsledku v původním jazyce

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 ?133p53 andp53? 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 ?133p53 and increased p53? 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 ?133p53 protein. In poorly proliferative, ?133p53-low CD8+CD28? cells, reconstituted expression of either ?133p53 or CD28 upregulated endogenous expression of each other, which restored cell proliferation, extended replicative lifespan and rescued senescence phenotypes

Název v anglickém jazyce

p53 isoforms regulate aging- and tumor-associated replicative senescence in T lymphocytes

Popis výsledku anglicky

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 ?133p53 andp53? 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 ?133p53 and increased p53? 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 ?133p53 protein. In poorly proliferative, ?133p53-low CD8+CD28? cells, reconstituted expression of either ?133p53 or CD28 upregulated endogenous expression of each other, which restored cell proliferation, extended replicative lifespan and rescued senescence phenotypes

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

The Journal of Clinical Investigation

ISSN

0021-9738

e-ISSN

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Svazek periodika

123

Číslo periodika v rámci svazku

12

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

5247-5257

Kód UT WoS článku

000327826100029

EID výsledku v databázi Scopus

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