Caspase-resistant vimentin suppresses apoptosis after photodynamic treatment with a silicon phthalocyanine in Jurkat cells

Oxidative stress, such as photodynamic therapy, is an apoptosis inducer. Ap optosis, as well as photosensitization, have been associated with disruptio n of the cytoskeletal network. The purpose of the present study was to asse ss the role of vimentin, a major cytoskeletal protein, in apoptosis after p hotodynamic treatment (PDT) with the silicon phthalocyanine Pc 4 in human J urkat T cells. Here we show for the first time that photosensitization with Pc 4 initiates vimentin cleavage and that this event precedes poly(ADP-rib ose) polymerase (PARP) degradation. Similar findings were obtained in the p resence of Ca-ceramide, an inducer of oxidative stress and apoptosis, In th e presence of benzyloxycarbonyl-Val-Ala-Asp(O-methyl)-fluoromethylketone, a pan-caspase inhibitor, Pc 4-PDT-induced vimentin and PARP cleavage were ab olished. In Jurkat cells transfected with a caspase-resistant vimentin apop tosis was partly suppressed and delayed post-Pc 4-PDT, We suggest that the full-length vimentin confers resistance to nuclear apoptosis after PDT with Pc 4. (C) 2001 Academic Press.