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Effects of BAPTA‐AM and Forskolin on Apoptosis and Cytochrome c Release in Photosensitized Chinese Hamster V79 Cells
Author(s) -
Inanami O.,
Yoshito A.,
Takahashi K.,
Hiraoka W.,
Kuwabara M.
Publication year - 1999
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1999.tb08265.x
Subject(s) - forskolin , apoptosis , cytochrome c , chinese hamster , chemistry , bapta , caspase 9 , caspase , microbiology and biotechnology , intracellular , biochemistry , biology , programmed cell death , receptor , in vitro
The mechanism of caspase‐3‐dependent apoptosis induced by photodynamic therapy (PDT) of cultured Chinese hamster V79 cells with pheophorbide a (PPa) was investigated. The PPa‐PDT induced rapid apoptosis within 30 min after irradiation of cells. This apoptosis was inhibited by the 1 O 2 quencher N 3 ‐ and caspase‐3 inhibitor acetyl‐Asp‐Glu‐Val‐Asp‐aldehyde, suggesting that 1 O 2 activated caspase‐3 and then caused apoptosis. The intracellular calcium [Ca 2+ ] 1 chelator (acetoxymethyl)‐l,2‐bis( o ‐aminophenoxy)ethane N , N , N ', N ,'‐tetraacetic acid (BAPTA‐AM) and the cyclic adenosine monophosphate (cAMP)‐increasing agent forskolin also inhibited not only the PPa‐PDT‐induced activation of caspase‐3 but also apoptosis in V79 cells. Furthermore, PPa‐PDT‐induced cytochrome c release from mitochondria was found to be inhibited by the treatment with BAPTA‐AM but not forskolin. These results indicated that [Ca 2+ ] 1 and cAMP independently serve as regulators for PPa‐PDT‐induced apoptosis in the upstream of caspase‐3.