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Recovery of Liver Sinusoidal Endothelial Cells Following Monocrotaline-induced Liver Injury

Authors
  • OTAKA, FUMISATO1, 2, 3
  • ITO, YOSHIYA1, 2
  • GOTO, TAKUYA1, 2, 4
  • KOJO, KEN4
  • TANABE, MINA1, 2, 3
  • HOSONO, KANAKO1, 2
  • MAJIMA, MASATAKA1, 2, 5
  • KOIZUMI, WASABURO3
  • AMANO, HIDEKI1, 2
  • 1 Department of Molecular Pharmacology, Graduate School of Medical Sciences,Kitasato University, Sagamihara, Japan
  • 2 Department of Pharmacology, Kitasato University School of Medicine, Sagamihara, Japan
  • 3 Department ofGastroenterology,Kitasato University School of Medicine, Sagamihara, Japan
  • 4 Department of Surgery,Kitasato University School of Medicine, Sagamihara, Japan
  • 5 Department of Medical Therapeutics, Kanagawa Institute of Technology, Atsugi, Japan
Type
Published Article
Journal
In Vivo
Publisher
International Institute of Anticancer Research
Publication Date
Sep 03, 2021
Volume
35
Issue
5
Pages
2577–2587
Identifiers
DOI: 10.21873/invivo.12540
PMID: 34410945
PMCID: PMC8408714
Source
PubMed Central
Keywords
Disciplines
  • Research Article
License
Unknown

Abstract

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.

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