Involvement of ASK1 activation in apoptosis induced by NPe6-PDT

被引：0

作者：

Liu, Lei ^{[1
]}

Zhang, Zhen-zhen ^{[1
]}

Zhang, Zhi-gang ^{[1
]}

机构：

[1] S China Normal Univ, MOE Key Lab Laser Life Sci, Guangzhou 510631, Guangdong, Peoples R China

来源：

BIOPHOTONICS AND IMMUNE RESPONSES V | 2010年 / 7565卷

关键词：

Photodynamic therapy (PDT); Apoptosis; ASK1; N-aspartyl chlorin e6 (NPe6); NEURONAL CELL-DEATH; PHOTODYNAMIC THERAPY; PATHWAYS; KINASE;

D O I：

10.1117/12.840472

中图分类号：

R318 [生物医学工程];

学科分类号：

0831 ;

摘要：

Photodynamic therapy (PDT) employing photosensiter N-aspartyl chlorin e6 (NPe6) can induce lysosome disruption and initiate apoptotic pathway. Apoptosis signal-regulating kinase (ASK1) is an important regulator of apoptosis in response to various stresses, such as reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, lipopolysaccharide (LPS) and calcium influx. In this study, we investigated the molecular mechanisms of apoptosis induced by NPe6-PDT in ASTC-a-1 cells. The results showed that the activities of ASK1 increased in response to NPe6-PDT. Over-expression of wild-type or activated mutant of ASK1 could obviously decrease cell viability and increase cell death; while inhibition of ASK1 significantly decreased cell apoptosis. These results suggested that ASK1 plays an important role in apoptosis induced by NPe6-PDT.

引用

页数：7

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