| ID | 110160 |
| Author |
Ito, Takanori
Department of Gastroenterology and Hepatology
Ishigami, Masatoshi
Department of Gastroenterology and Hepatology
Matsushita, Yoshihiro
Department of Oral and Maxillofacial Surgery of Nagoya University Graduate School of Medicine
Hirata, Marina
Department of Oral and Maxillofacial Surgery of Nagoya University Graduate School of Medicine
Matsubara, Kohki
Department of Oral and Maxillofacial Surgery of Nagoya University Graduate School of Medicine
Ishikawa, Tetsuya
Department of Gastroenterology and Hepatology
Hibi, Hideharu
Department of Oral and Maxillofacial Surgery of Nagoya University Graduate School of Medicine
Ueda, Minoru
Department of Oral and Maxillofacial Surgery of Nagoya University Graduate School of Medicine
Hirooka, Yoshiki
Department of Gastroenterology and Hepatology
Goto, Hidemi
Department of Gastroenterology and Hepatology
Yamamoto, Akihito
Department of Oral and Maxillofacial Surgery of Nagoya University Graduate School of Medicine|Department of Oral histology, Institute of Biomedical Science, Tokushima University Graduate School
Tokushima University Educator and Researcher Directory
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| Content Type |
Journal Article
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| Description | Effective treatments for acute liver failure (ALF) are still lacking. We recently reported that a single intravenous administration of serum-free conditioned medium from stem cells derived from human exfoliated deciduous teeth (SHED-CM) into the D-galactosamine (D-Gal)-induced rat ALF model improves the liver injury. However, the specific factors in SHED-CM that are responsible for resolving ALF remain unclear. Here we found that depleting SHED-CM of two anti-inflammatory M2 macrophage inducers—monocyte chemoattractant protein-1 (MCP-1) and the secreted ectodomain of sialic acidbinding Ig-like lectin-9 (sSiglec-9)—abolished its ability to resolve rat ALF. Furthermore, treatment with MCP-1/sSiglec-9 alone dramatically improved the survival of ALF rats. This treatment induced anti-inflammatory M2, suppressed hepatocyte apoptosis, and promoted hepatocyte proliferation. Treatment with an M2-depletion reagent (mannosylated clodronate liposomes) suppressed the recovery. In addition, MCP-1 and sSiglec-9 synergistically promoted the M2 differentiation of bone marrow-derived macrophages via CCR2, accompanied by the production of multiple liver-regenerating factors. The conditioned medium from MCP-1/sSiglec-9-activated M2 macrophages, but not from interleukin-4-induced ones, suppressed the D-Gal- and LPS-induced apoptosis of primary hepatocytes and promoted their proliferation in vitro. The unique combination of MCP-1/sSiglec-9 ameliorates rat ALF by inhibiting hepatocellular apoptosis and promoting liver regeneration through the induction of anti-inflammatory/tissue-repairing M2 macrophages.
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| Journal Title |
Scientific Reports
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| ISSN | 20452322
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| Publisher | Springer Nature
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| Volume | 7
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| Start Page | 44043
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| Sort Key | 44043
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| Published Date | 2017-03-08
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| Remark | © The Author(s) 2017 This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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| EDB ID | |
| DOI (Published Version) | |
| URL ( Publisher's Version ) | |
| FullText File | |
| language |
eng
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| TextVersion |
Publisher
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| departments |
Oral Sciences
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