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

Abstract

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 Vfluorescein isothiocyanate (FITC) and mitochondrial membrane potential was measured by 5,5?,6,6?-tetrachloro-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.

Pharmacological and Genetic Inhibition of Translocator Protein 18 kDa Ameliorated Neuroinflammation in Murine Endotoxemia Model

“…However, we observed that ONO-2952 effectively suppressed LPS-induced IL-1β mRNA expression in the hippocampus, whereas the germ-line knockout of TSPO did not suppress this cytokine in the present study. As TSPO is expressed as early as the preimplantation embryonic stage (27), a compensatory mechanism modifying the inflammatory response in the brain may occur during development. Although wild-type and knockout mice shared the same genetic background, i.e., C57BL/6J, and kept in the same environment at least 7 days before we started the experiment, we could not exclude the possibility that the growth environment contributed to the phenotypic difference between wild type and TSPOKO.…”