Characterization of adipose tissue-derived stromal cells of mice with nonalcoholic fatty liver disease and their use for liver repair.

AST, aspartate aminotransferase AT-HF, atherogenic high-fat Adipose tissue FCM, flow cytometry HICs, hepatic inflammatory cells LD, lactate dehydrogenase MSCs, mesenchymal stem cells Mesenchymal stem cells NAFLD, nonalcoholic fatty liver disease NAS, NAFLD activity score NASH (12 w) u-ADSCs, NASH (12 weeks)-derived u-ADSCs NASH (4w) u-ADSCs, NASH (4 weeks)-derived u-ADSCs NASH, nonalcoholic steatohepatitis Non-alcoholic fatty liver disease Stromal cells qRT-PCR, quantitative real-time polymerase chain reaction u-ADSCs, uncultured adipose tissue-derived stromal cells

Journal

Regenerative therapy
ISSN: 2352-3204
Titre abrégé: Regen Ther
Pays: Netherlands
ID NLM: 101709085

Informations de publication

Date de publication:
Dec 2021
Historique:
received: 03 08 2021
revised: 01 11 2021
accepted: 18 11 2021
entrez: 20 12 2021
pubmed: 21 12 2021
medline: 21 12 2021
Statut: epublish

Résumé

Freshly isolated uncultured adipose tissue-derived stromal cells (u-ADSCs), containing miscellaneous cells like the relatively abundant mesenchymal stem cells, are attractive for repair and regenerative therapy. However, the detailed characteristics and therapeutic efficacy of u-ADSCs obtained from disease-affected hosts are unknown. We compared the properties of u-ADSCs obtained from wild-type mice and from a mouse model of non-alcoholic steatohepatitis (NASH). The NASH model was established by feeding C57BL/6J mice an atherogenic high-fat diet for 4 (NASH (4w)) or 12 weeks (NASH (12w)), followed by the isolation and characterization of u-ADSCs. Wild-type u-ADSCs or NASH-derived u-ADSCs were administered to mice with NASH cirrhosis, followed by analyses of hepatic inflammatory cells, antigen profiles, fibrosis, and gene expression. Wild-type u-ADSCs and NASH-derived u-ADSCs did not show marked differences in surface antigen profiles. In NASH (4w) u-ADSCs, but not NASH (12w) u-ADSCs, the frequencies of the leukocyte markers CD11b, CD45, and CD44 were elevated; furthermore, we observed an increase in the M1/M2 macrophage ratio only in NASH (12w) u-ADSCs. Only in NASH-4w u-ADSCs, the expression levels cell cycle-related genes were higher than those in u-ADSCs. Wild-type u-ADSCs administered to mice with NASH-related cirrhosis decreased the infiltration of CD11b+, F4/80+, and Gr-1+ inflammatory cells, ameliorated fibrosis, and had a restorative effect on liver tissues, as determined by gene expression profiles and the NAFLD activity score. The therapeutic effects of NASH (4w) u-ADSCs and NASH (12w) u-ADSCs on NASH-related cirrhosis were highly similar to the effect of wild-type u-ADSCs, including reductions in inflammation and fibrosis. NASH-derived u-ADSCs, similar to wild-type u-ADSCs, are applicable for reparative and regenerative therapy in mice with NASH.

Identifiants

pubmed: 34926735
doi: 10.1016/j.reth.2021.11.005
pii: S2352-3204(21)00087-0
pmc: PMC8649123
doi:

Types de publication

Journal Article

Langues

eng

Pagination

497-507

Informations de copyright

© 2021 The Japanese Society for Regenerative Medicine. Production and hosting by Elsevier B.V.

Déclaration de conflit d'intérêts

None declared.

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Auteurs

Masaaki Yano (M)

Department of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.

Alessandro Nasti (A)

System Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.

Akihiro Seki (A)

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Kosuke Ishida (K)

System Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.

Masatoshi Yamato (M)

Department of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.

Hiiro Inui (H)

Department of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.

Norihiko Ogawa (N)

System Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.

Shingo Inagaki (S)

System Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.

Tuyen Thuy Bich Ho (TTB)

System Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.

Kazunori Kawaguchi (K)

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Taro Yamashita (T)

Department of General Medicine, Kanazawa University Hospital, Kanazawa, Japan.

Kuniaki Arai (K)

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Tatsuya Yamashita (T)

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Eishiro Mizukoshi (E)

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Oto Inoue (O)

Department of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.

Shinichiro Takashima (S)

Department of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.

Soichiro Usui (S)

Department of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.

Masayuki Takamura (M)

Department of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.

Masao Honda (M)

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Takashi Wada (T)

Department of Nephrology and Laboratory Medicine, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.

Shuichi Kaneko (S)

Department of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
System Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.
Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Yoshio Sakai (Y)

Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.

Classifications MeSH