In conclusion, the expression of PAR6 was observed in cysts when somatic cells began to invade at 17.5 dpc, and became strong in the nuclei of all primordial follicular oocytes at3 dpp. On the other hand, it obviously decreased when the primordial follicles were recruited into the Sertindole population of growing follicles. Inhibition of PAR6 by antiPAR6 antibody, RNA interference, and CBX blocked the formation of primordial follicles. CBX also inhibited the expression of PAR6. These results indicate that the expression of PAR6 in female mouse germ cells may have new roles in contributing to the formation of primordial follicles and the maintenance of oocyte arrest at the diplotene stage. Maybe it could serve as a marker for the germ cells to be selected to form the primordial follicles. A thorough investigation of PAR6 will be useful to reveal the mechanism of primordial follicle formation and maintenance. Pulmonary fibrosis is a devastating disorder that is resistant to treatment. Initial injury to the lung causes the recruitment of inflammatory cells, release of cytokines, and eventual increase in fibroblast activity, Salirasib leading to parenchymal remodeling and, finally, fibrosis. Although various cytokines and growth factors are involved in these responses, transforming growth factor is known to play the most essential role in the pathogenesis of lung fibrosis. Sphingosine-1-phosphate is a bioactive sphingolipid metabolite involved in many critical cellular processes, including proliferation, differentiation, migration, and angiogenesis, through interaction with a family of five G protein�Ccoupled receptors . In dendritic cells, S1P3 is reported to play a critical role in regulating inflammation in sepsis syndrome via cross-talk with PAR1. S1P3 also mediates the chemotactic effects of S1P in macrophages in vitro and in vivo, and plays a causal role in atherosclerosis by promoting inflammatory monocyte/macrophage recruitment. With regard to S1P receptor profiles in neutrophils, S1P1, S1P4, and S1P5 are reported to be expressed on neutrophils in both patients with pneumonia and healthy subjects, while S1P3 receptor expression is observed only on neutrophils from patients with pneumonia.