TY - JOUR T1 - Recovery of Liver Sinusoidal Endothelial Cells Following Monocrotaline-induced Liver Injury JF - In Vivo JO - In Vivo SP - 2577 LP - 2587 DO - 10.21873/invivo.12540 VL - 35 IS - 5 AU - FUMISATO OTAKA AU - YOSHIYA ITO AU - TAKUYA GOTO AU - KEN KOJO AU - MINA TANABE AU - KANAKO HOSONO AU - MASATAKA MAJIMA AU - WASABURO KOIZUMI AU - HIDEKI AMANO Y1 - 2021/09/01 UR - http://iv.iiarjournals.org/content/35/5/2577.abstract N2 - 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. ER -