Objective: Hepatic sinusoidal obstruction syndrome (SOS) induced by chemotherapy or hematopoietic stem cell transplantation causes severe liver injury. Although the pathology of SOS is characterized by damage to liver sinusoidal endothelial cells (LSECs), the processes underlying LSEC repair are incompletely understood. The purpose of this study was to clarify the regeneration process of damaged hepatic sinusoidal endothelial cells in SOS. 
Methods and Results: A SOS model was created by intraperitoneal administration of monocrotaline (MCT) to male C57BL/6 mice. ALT levels peaked at 48 h post-MCT administration and necrosis occurred around the central veins, but recovered to normal at 120 h. The hepatic expression of EC damage markers increased after 48 h and was also accompanied by intrahepatic hemorrhage. Thereafter, EC damage markers decreased with hepatic repair, and the hepatic sinusoidal structure was reconstructed. LYVE-1 mRNA expression, an LSEC marker, increased during the liver repair phase. LYVE-1 expression around the central veins was weak before treatment and further decreased at 48 h, but increased at 96 h and 120 h. Bone marrow-derived cells did not incorporate into the restored LYVE-1-positive cells.  
Conclusions: These results suggested that the regenerating endothelium was thought to be due to endothelial proliferation in the vicinity of the injury, and that bone marrow-derived cells are unlikely to be involved.