The tumor suppressor p53 can translocate into mitochondria and activate apoptosis. Here we studied whether p53 mitochondrial translocation and subsequent apoptosis were affected by blocking mitochondrial permeability transition pore using cyclosporine A (CsA) and bongkrekic acid (BA) in skin epidermal JB6 cells and skin tissues. Our results demonstrated that CsA and BA blocked TPA-induced p53 translocation, leading to protection against the loss of mitochondrial membrane potential and Complex I activity, and eventually suppression of apoptosis. Thus, our results suggest that mitochondrial permeability transition is required for p53 mitochondrial translocation.
|Number of pages||6|
|State||Published - Apr 16 2008|
Bibliographical noteFunding Information:
The authors wish to thank Dr. Nancy Colburn at NCI/NIH for providing us the mouse skin epidermal JB6 cells; Kathleen Llorens at LSU Health Sciences Center-Shreveport Research Core Facility for technical support in laser confocal experiments; Dr. Steven Pruett at LSUHSC-S for technical support on VersaDoc Imagine System; Dr. Tammy Dugas, Dr. Kenneth McMartin, Dr. Heather Kleiner, Bo Jiang, and Yan Li at LSUHSC-S for their technical supports. This work was supported in part by Grant Number R03CA128077 from the National Cancer Institute.
ASJC Scopus subject areas
- Structural Biology
- Molecular Biology
- Cell Biology