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Adaptive responses is differently induced depending on the sensitivity to radiation induced cell death in mouse epidermal cells

Authors
 S.J. Lee  ;  S.A. Choi  ;  C.K. Cho  ;  T.H. Kim  ;  K.S. Jeong  ;  S.Y.Yoo  ;  Y.S. Lee 
Citation
 Cell Biology and Toxicology, Vol.16(3) : 175-184, 2000 
Journal Title
 Cell Biology and Toxicology 
ISSN
 0742-2091 
Issue Date
2000
MeSH
Adaptation, Physiological/radiation effects ; Animals ; Apoptosis/radiation effects* ; Cell Line, Transformed ; Cytosol/enzymology ; Epidermal Cells* ; Epidermis/radiation effects* ; In Situ Nick-End Labeling ; Isoenzymes/metabolism ; Keratinocytes/cytology* ; Keratinocytes/enzymology ; Keratinocytes/radiation effects* ; Mice ; Mice, Inbred BALB C ; Papilloma ; Protein Kinase C/metabolism ; Protein Kinase C-alpha ; Radiation Dosage ; Radiation Injuries/metabolism ; Skin Neoplasms ; Tumor Cells, Cultured ; ras Proteins/metabolism
Keywords
adaptive response ; normal cells ; neoplastic cells ; protein kinase C ; cell death
Abstract
We investigated the relationship between induction of radio-adaptive response and cell death in mouse normal and neoplastic epidermal cells. Mouse normal primary keratinocytes (PK), cancer-prone cells [v-rasHa-transfected mouse keratinocytes (ras-PK), and line 308 cells (mouse skin papilloma cells which have activated rasHa gene with A-to-T transversion at codon 61) were primed with a low dose of gamma-rays (0.01 Gy), and were challenged with a high dose (4 Gy) after a 4 or 7 h interval. The induction of cell death in PK was 2-10 times higher and was also more rapid in PK than in ras-PK or 308 cells. Low-dose pretreatment with a 4 h interval decreased cell death, and this adaptive response was prominent in PK, whereas it was less obvious in the cases of ras-PK and 308 cells. The response of each protein kinase C (PKC) isozymes to high-dose radiation, especially PKCalpha, PKCdelta, PKCepsilon, and PKCeta, were different between the normal and ras oncogene-activated neoplastic keratinocytes; translocation of these isozymes to membrane occurred more rapidly in normal than in neoplastic cells. Furthermore, low-dose pretreatment did not induce the translocation of PKCdelta in PK significantly more than in ras-PK and 308. Thus, the difference in the induction of radio-adaptive responses between mouse normal and neoplastic epidermal cells reflects difference in the rapidity of cell death, and responsiveness of PKC may affect this adaptive response.
Full Text
https://link.springer.com/article/10.1023/A:1007658905639
DOI
10.1023/a:1007658905639
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers
Yonsei Authors
Lee, Yun Sil(이윤실)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/171738
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