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Apoptotic Signaling Cascade of 5-aminolaevulinic Acid-based Photodynamic Therapy in Human Promyelocytic Leukemia HL-60 Cells
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  • Apoptotic Signaling Cascade of 5-aminolaevulinic Acid-based Photodynamic Therapy in Human Promyelocytic Leukemia HL-60 Cells
  • Apoptotic Signaling Cascade of 5-aminolaevulinic Acid-based Photodynamic Therapy in Human Promyelocytic Leukemia HL-60 Cells
저자명
Nagao. Tomokazu,Matsuzaki. Kazuki,Takahashi. Miho,Minamitani. Haruyuki
간행물명
Journal of photoscience: an international journal officail organ of the Korean Society of Photoscience
권/호정보
2002년|9권 2호|pp.509-511 (3 pages)
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한국광과학회
파일정보
정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

In this study, we investigated apoptotic cell death induced by photodynamic therapy using 5-aminolaevulinic acid (ALA-PDT) in human promyelocytic leukemia cells (HL-60). ALA-PDT induced apoptosis in HL-60 cells as confirmed by DNA agarose gel electrophoresis and nuclear staining with Hoechst 33342. The apoptotic cell death was inhibited by addition of broad-spectrum caspase inhibitor Z-Asp-CH$_2$-DCB, indicating that the apoptotic cell death was induced in a caspase-dependent manner. Actually, western blotting analysis revealed that caspase-3 was processed as early as 1.5 h after ALA-PDT. Cytoplasmic cytochrome c released from mitochondria was detected by western blotting. However, inhibitor of caspase-9, a cysteine protease located in the downstream of cytochrome c release, was not able to reduce the apoptotic cell death. Therefore, the mitochondrial apoptotic pathway was not involved in the ALA-PDT-induced apoptosis. On the other hand, it was found that ALA-PDT-induced apoptosis was clearly inhibited by pretreatment of caspase-8 inhibitor. These data suggest that caspase-8-mediated apoptotic pathway is important in ALA-PDT-induced cell death.