Please use this identifier to cite or link to this item:
|Title:||Programmed cell death in Blastocystis hominis occurs independently of caspase and mitochondrial pathways|
|Authors:||Nasirudeen, A.M.A. |
Programmed cell death
|Source:||Nasirudeen, A.M.A., Tan, K.S.W. (2005). Programmed cell death in Blastocystis hominis occurs independently of caspase and mitochondrial pathways. Biochimie 87 (6) : 489-497. ScholarBank@NUS Repository. https://doi.org/10.1016/j.biochi.2005.03.003|
|Abstract:||We demonstrated previously that a cytotoxic monoclonal antibody (MAb) 1D5 elicits a programmed cell death (PCD) response in Blastocystis hominis and showed that caspase-3-like protease influences but is not essential for PCD in MAb 1D5-treated B. hominis. We also showed that mitochondrial dysregulation played a role in cell death. In the current study, we further analyzed the signaling pathways involved in PCD mediated by MAb 1D5. B. hominis cells were treated with MAb 1D5 or control MAb 5, either with or without pretreatment with a pan-caspase inhibitor, zVAD.fmk, and/or a mitochondrial transition pore blocker, cyclosporine A (CA). Flow cytometric examination of cell size, mitochondrial membrane potential (ΔΨm), caspase activation and in situ DNA fragmentation showed that zVAD.fmk and CA, used independently or in combination, failed to inhibit MAb 1D5-mediated PCD. Interestingly, cell exposure to either inhibitor resulted in partial inhibition of DNA fragmentation while combined exposure of cells to inhibitors abolished DNA fragmentation completely. This study sheds new light on the conserved nature of PCD pathways in parasitic protozoa and is also the first report describing caspase- and mitochondria-independent cell death pathways in a protozoan parasite. © 2005 Elsevier SAS. All rights reserved.|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Dec 6, 2017
WEB OF SCIENCETM
checked on Nov 22, 2017
checked on Dec 17, 2017
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.