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作 者:FEIFAN ZHOU DA XING WEI R.CHEN
机构地区:[1]MOE Key Laboratory of Laser Life Science&Institute of Laser Life Science South China Normal University,Guangzhou 510631,China [2]Department of Engineering and Physics,College of Mathematics and Science University of Central Oklahoma,Edmond,Oklahoma 73034,USA
出 处:《Journal of Innovative Optical Health Sciences》2009年第2期209-214,共6页创新光学健康科学杂志(英文)
基 金:the National Natural Science Foundation of China(30627003,30870676,30870658);the Natural Science Foundation of Guangdong Province(7117865);as well as by a grant from the US National Institute of Health(P20 RR016478 from the INBRE Program of the National Center for Research Resources).
摘 要:Apoptosis is an important cellular event that plays a key role in the therapy of many diseases.The mechanism of the initiation and regulation of photodynamic therapy(PDT)–induced apoptosis is complex.Our previous study found that Photofrin was localized primarily in mitochondria,the primary targets of Photofrin-PDT.The key role of Bax in the mitochondria-mediated apoptosis has been demonstrated in many systems.In order to determine the role of Bax in the mitochondrion-mediated apoptosis induced by Photofrin-PDT,we used the GFP-Bax plasmid to monitor the dynamics of Bax activation after PDT treatment.With laser scanning confocal microscopy,we found that Bax did not translocate from the cytosol to mitochondria when the mitochondrial membrane potential(∆Ψm)disappeared,measured by TMRM.Thus,for Photofrin-PDT,the commitment to cell death is independent of Bax activation.
关 键 词:Photofrin-photodynamic therapy mitochondria-mediated apoptosis BAX activation translocation.
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