ZANNI, Giulia, Elena DI MARTINO, Anna OMELYANENKO, Michael ANDÄNG, Ulla DELLE, Kecke ELMROTH a Klas BLOMGREN. Lithium increases proliferation of hippocampal neural stem/progenitor cells and rescues irradiation-induced cell cycle arrest in vitro. Oncotarget. Albany: Impact Journals, 2015, roč. 6, č. 35, s. 37083-37097. ISSN 1949-2553.
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Základní údaje
Originální název Lithium increases proliferation of hippocampal neural stem/progenitor cells and rescues irradiation-induced cell cycle arrest in vitro
Autoři ZANNI, Giulia (752 Švédsko), Elena DI MARTINO (752 Švédsko), Anna OMELYANENKO (752 Švédsko), Michael ANDÄNG (752 Švédsko, garant, domácí), Ulla DELLE (752 Švédsko), Kecke ELMROTH (752 Švédsko) a Klas BLOMGREN (752 Švédsko).
Vydání Oncotarget, Albany, Impact Journals, 2015, 1949-2553.
Další údaje
Originální jazyk angličtina
Typ výsledku Článek v odborném periodiku
Obor 30200 3.2 Clinical medicine
Stát vydavatele Spojené státy
Utajení není předmětem státního či obchodního tajemství
WWW URL
Impakt faktor Impact factor: 5.008
Kód RIV RIV/00216224:14740/15:00087265
Organizační jednotka Středoevropský technologický institut
UT WoS 000366113200014
Klíčová slova anglicky lithium; hippocampus; radiotherapy; apoptosis; paediatric oncology
Štítky rivok
Změnil Změnila: Mgr. Eva Špillingová, učo 110713. Změněno: 13. 4. 2016 10:14.
Anotace
Radiotherapy in children causes debilitating cognitive decline, partly linked to impaired neurogenesis. Irradiation targets primarily cancer cells but also endogenous neural stem/progenitor cells (NSPCs) leading to cell death or cell cycle arrest. Here we evaluated the effects of lithium on proliferation, cell cycle and DNA damage after irradiation of young NSPCs in vitro. NSPCs were treated with 1 or 3 mM LiCl and we investigated proliferation capacity (neurosphere volume and bromodeoxyuridine (BrdU) incorporation). Using flow cytometry, we analysed apoptosis (annexin V), cell cycle (propidium iodide) and DNA damage (gamma H2AX) after irradiation (3.5 Gy) of lithium-treated NSPCs. Lithium increased BrdU incorporation and, dose-dependently, the number of cells in replicative phase as well as neurosphere growth. Irradiation induced cell cycle arrest in G(1) and G(2)/M phases. Treatment with 3 mM LiCl was sufficient to increase NSPCs in S phase, boost neurosphere growth and reduce DNA damage. Lithium did not affect the levels of apoptosis, suggesting that it does not rescue NSPCs committed to apoptosis due to accumulated DNA damage. Lithium is a very promising candidate for protection of the juvenile brain from radiotherapy and for its potential to thereby improve the quality of life for those children who survive their cancer.
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