Apoptosis is an important cellular event that plays a key role in therapy of many diseases. The mechanisms of the
initiation and regulation of photodynamic therapy (PDT) -induced apoptosis is complex. Some PDT-associated
apoptosis pathways involved plasma membrane death receptors, mitochondria, lysosomes and endoplasmic reticulum
(ER). Our previous study found that Photofrin were localized primarily in mitochondria, the primary targets of
Photofrin-PDT. The key role of Bax in the mitochondrion-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
CFP/GFP-Bax plasmid to monitor the dynamics of Bax activation and translocation after PDT treatment. With laser
scanning confocal microscopy, we found that PDT induced Bax translocation from the cytosol to mitochondria; however,
with cells over-expressing YFP-HSP70 plasmids, Bax translocation was not detected. Thus, for Photofrin-PDT, Bax
activation and translocation were inhibited by HSP70, not influence the cell death.