Steroidogenic acute regulatory protein (StAR) and peripheral-type benzodiazepine receptor (PBR) are decreased in human apoptotic embryos

Fragmentation in human pre-implantation embryos has been suggested as the process of apoptosis. We have previously demonstrated a direct relationship between the increased reactive oxygen species (ROS) and apoptosis in human pre-implantation embryos. ROS is known to suppress the function of mitochondria in which steroidogenic acute regulatory protein (StAR) and peripheral-type benzodiazepine receptor (PBR) are presented. Therefore, the purpose of this study was to examine the expression of StAR and PBR in human pre-implantation embryos and to evaluate whether reduction of these proteins is associated with apoptosis. Apoptosis was detected by annexin V-fluorescein isothiocyanate (FITC) and mitochondrial membrane potential was measured by 5,5',6,6'-tetrachlorol, 1,1',3,3'-tetraethyl-benzimidazolyl-carbocyanine iodide (JC-1). Immunofluorescence staining and Western blotting were applied to examine the expression of StAR and PBR in the embryos. Lipid droplets in the embryos were stained with Oil Red O. The fragmented pre-implantation embryos were stained with annexin V-FITC, but not the normal ones. The mitochondria with active membrane potential were present less in the fragmented embryos compared with the non-fragmented embryos. We also confirmed that both StAR and PBR were expressed in the embryos and their expression levels were lower in the fragmented ones. In addition, the number and size of lipid droplets were increased in the fragmented embryos. The present study provides evidence that reduction of StAR and PBR in human preimplantation embryos is associated with an increase in the lipid droplets leading to apoptosis.