International journal of radiation biology · 2002
Adaptive response and the influence of ageing: effects of low-dose irradiation on cell growth of cultured glial cells.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Miura Y, Abe K, Urano S, Furuse T, Noda Y, Tatsumi K, Suzuki S
Аннотация
PURPOSE: To examine the molecular mechanism of radiation adaptive response (RAR) for the growth of cultured glial cells and to investigate the influence of ageing on the response.
MATERIALS AND METHODS: Glial cells were cultured from young and older rats (1 and 24 months). RAR for the growth of glial cells conditioned with a low dose of X-rays and subsequently exposed to a high dose of X-rays was examined for cell number and BrdU incorporation. Involvement of the subcellular signalling pathway factors in RAR was investigated using their inhibitors, activators, and mutated and knockout glial cells.
RESULTS: RAR was observed in cells cultured from young rats but was not in cells from older animals. The inhibitors of protein kinase C (PKC) and DNA-dependent protein kinase (DNA-PK) or phosphatidylinositol 3-kinase (PI3K) suppressed RAR. The activators of PKC instead of low-dose irradiation also caused RAR. Moreover, glial cells cultured from severe combined immunodeficiency (scid) mice (CB-17 scid) and ataxia-telangiectasia mutated (Atm) knockout mice showed no RAR.
CONCLUSION: The results indicated that PKC, ATM, DNAPK and/or PI3K were involved in RAR for growth and BrdU incorporation of cultured glial cells and RAR decreased with ageing.
MATERIALS AND METHODS: Glial cells were cultured from young and older rats (1 and 24 months). RAR for the growth of glial cells conditioned with a low dose of X-rays and subsequently exposed to a high dose of X-rays was examined for cell number and BrdU incorporation. Involvement of the subcellular signalling pathway factors in RAR was investigated using their inhibitors, activators, and mutated and knockout glial cells.
RESULTS: RAR was observed in cells cultured from young rats but was not in cells from older animals. The inhibitors of protein kinase C (PKC) and DNA-dependent protein kinase (DNA-PK) or phosphatidylinositol 3-kinase (PI3K) suppressed RAR. The activators of PKC instead of low-dose irradiation also caused RAR. Moreover, glial cells cultured from severe combined immunodeficiency (scid) mice (CB-17 scid) and ataxia-telangiectasia mutated (Atm) knockout mice showed no RAR.
CONCLUSION: The results indicated that PKC, ATM, DNAPK and/or PI3K were involved in RAR for growth and BrdU incorporation of cultured glial cells and RAR decreased with ageing.
Предметные рубрики MeSH
Age FactorsAgingAnimalsBromodeoxyuridineCell DivisionCells, CulturedDNA-Activated Protein KinaseDNA-Binding ProteinsDose-Response Relationship, RadiationEnzyme InhibitorsFemaleMiceMice, KnockoutMice, SCIDNeurogliaPhosphatidylinositol 3-KinasesProtein Kinase CProtein Serine-Threonine KinasesRatsRats, WistarSignal TransductionTime FactorsX-Rays