Induction of p21Cip1-mediated G2/M arrest in H2O2-treated lens epithelial cells.

作者: Jong-Tak Kim , Young Seomun , Ji-Young Park , Hae-Sook Kim , Choun-Ki Joo

DOI:

关键词: Oxidative stressCell cycleCell Cycle GeneCyclin-dependent kinase 1Cell biologyCell typeTransfectionCell cycle checkpointSenescenceChemistry

摘要: PURPOSE Oxidative damage is one of the major factors associated with formation age-related cataract and senescence various cell types. Although effects oxidative stress are complex, we focused on whether affects control cycle in lens epithelial cells. METHODS BrdU labeling FACS analysis were used to investigate effect H2O2 HLE B-3 In addition, western Northern blot performed assess expression regulatory proteins transfection siRNA was knock out p21Cip1. The activation MAPK family members by assessed using antibodies detect activated forms. To confirm an ex vivo model, its cultures lenses 3-week-old SD rats examined. localization PCNA p21Cip1 rat analyzed immunohistochemistry. RESULTS showed that treatment induced G2/M phase arrest strongly H2O2, whereas other genes unchanged. Attenuation reduced arrest. Furthermore, JNK ERK their specific inhibitors SP600125 (for JNK) U0126 ERK1/2) prevented blocked a organ culture also caused increase However, lowered levels p27Kip1, cdc2, culture, unlike CONCLUSIONS accumulation exposed may play role as defensive mediator damage, indicator for or aging, inducer cataract. This finding links p21Cip1-mediated

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