%0 Journal Article %A FUMISATO OTAKA %A YOSHIYA ITO %A TAKUYA GOTO %A KEN KOJO %A MINA TANABE %A KANAKO HOSONO %A MASATAKA MAJIMA %A WASABURO KOIZUMI %A HIDEKI AMANO %T Recovery of Liver Sinusoidal Endothelial Cells Following Monocrotaline-induced Liver Injury %D 2021 %R 10.21873/invivo.12540 %J In Vivo %P 2577-2587 %V 35 %N 5 %X Background/Aim: Although the pathology of sinusoidal obstruction syndrome (SOS) is characterized by damage to liver sinusoidal endothelial cells (LSECs), the processes underlying LSEC repair are incompletely understood. The angiopoietin (Ang)/Tie system contributes to angiogenesis. The present study aimed to examine the processes of LSEC repair and the involvement of the Ang/Tie pathway in LSEC recovery. Materials and Methods: Experimentally, SOS was induced by intraperitoneal injection of monocrotaline (MCT) to C57/BL6 mice. Results: Levels of LSEC markers were up-regulated during the repair phase of MCT-induced hepatotoxicity. The damaged LSECs recovered from the injury by expanding LSECs expressing lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) in the peri-central area of MCT-injured livers, while LSECs in the same area of uninjured livers lacked LYVE-1 expression. Bone marrow (BM)-derived cells did not incorporate into the restored LSECs. Tie2 expression was related to LSEC recovery in MCT-injured liver tissue. Conclusion: The resident LSECs neighboring uninjured tissue replace damaged LSECs in MCT-injured livers. Tie2 is involved in LSEC recovery from MCT-induced hepatotoxicity. %U https://iv.iiarjournals.org/content/invivo/35/5/2577.full.pdf