Trichomonas vaginalis-induced apoptosis in RAW264.7 cells is regulated through Bcl-xL, but not Bcl-2.

The purpose of this study was to determine whether anti-apoptotic proteins of the Bcl-2 family such as Bcl-2 and Bcl-x(L), proteins that confer resistance to apoptotic death from some stimuli, block apoptotic cell death in RAW264.7 cells upon treatment with Trichomonas vaginalis. In this study, the expression level of Bcl-2 was unchanged throughout the course of apoptotic cell death, and overexpressed Bcl-2 did not prevent release of cytochrome c, the significant change of the membrane potential, activation of caspases, and PARP cleavage in T. vaginalis-treated RAW264.7 cells. On the other hand, Bcl-x(L)expression was decreased after T. vaginalis treatment accompanied with Bax activation. Furthermore, we showed that release of mitochondrial cytochrome c, cleavage of caspase-9 and PARP during apoptosis in T. vaginalis-treated RAW264.7 cells were considerably diminished by transfection with overexpressed Bcl-x(L), and overexpressed Bcl-x(L)could inhibit T. vaginalis-induced apoptosis in RAW264.7 cells. In addition, interestingly, pre-treatment with caspase inhibitors, Boc-D-FMK and Z-DEVD-FMK, significantly abolished T. vaginalis-induced down-regulation of Bcl-x(L), suggesting that caspase-3 may play a pivotal role in the process of apoptosis as well as the down-regulation of Bcl-x(L)by T. vaginalis. Therefore, these results suggest that T. vaginalis-induced apoptosis in RAW264.7 cells can occur via a Bcl-x(L)-dependent apoptotic mechanism.