• The Journal of the Korean dental association
• /
• v.40 no.12 s.403
• /
• pp.917-927
• /
• 2002

• Journal of Life Science
• /
• v.7 no.1
• /
• pp.66-72
• /
• 1997

The term of apoptosis, programmed cell death, was firstly coined to distinguish with necrosis, pathologic cell death, by Kerr in 1972. Although various pathogenic factors are able to occur apoptosis, ti is essential process for normal development and physiology in the animals. Recently in the field of medicine, apoptosis researeh is especially focused in serveral Kind of pathopoiesis problems including cancer, immunodeficiency associated HIV and other virus, autommunity, alzheimer and congenital anormality. The information obtained from the animal model system for apoptosis should be directly applicable to both life science for understanding of development and medicine for practical the rapy. To know the common mechanism of apoptosis, it is prerequisite that the genes and factors responsible for apoptosis should be defined and characterized on the molecular level. The study of apoptosis should contribute largely to biology inculuding cell physiology and development, and both basic and clinical medicine to understand cause of diseases for therapy as well as congenital defect.

• Animal cells and systems
• /
• v.5 no.1
• /
• pp.77-83
• /
• 2001

The present study was conducted to elucidate whether the expression level of poly(ADP-ribose) polymerase (PARP) is related to the ultraviolet radiation (UV)-induced apoptosis. After treatment of the mammalian cell lines HeLa S3 and Chinese hamster ovary (CHO) with 50 J/m2 UV, induction of apoptosis was determined by several means during 24 h post-incubation. Incidence of apoptosis was much lower in CHO than HeLa S3 cells based on the percentage of apoptotic cells in terms of morphological changes in nucleus or direct counting of viable cells and qualitative or quantitative DNA fragmentation. Interestingly, when the expression level of PARP was measured by western blotting, the amounts of PARP that was retained at each time point inversely correlated with the incidences of apoptosis in these cells. Concomitant with generation of the 85 kDa fragment, 116 kDa PARP disappeared in HeLa S3 within 6 h after UV treatment, whereas a fair amounts of 116 kDa band was still retained in CHO cells at 36 h post-incubation. This inverse relationship was also observed in the adaptive response system, in which cells weve treated with a high dose of UV after pretreatment with a low dose. As expected, typical adaptive responses appeared in CHO cells but not in HeLa cells, showing greater cell viability and lesser DNA fragmentation. During the adaptive response in CHO cells, PARP was expressed at much higher level compared to the single, high dose-treated cells. Interestingly, even though PARP was induced at 6 h post-incubation In both cell types, its expression was more prominent in CHO cells. Thus, our data indicate that the retained level of intact PARP against UV damage inversely correlates with incidence of apoptosis in mammalian cells, and also suggest that a machinery to protect the PARP degradation against UV damage exists in CHO but not in HeLa S3 cells.