Evidence map›Paper›PMID 34926735›Full record

ArticleRegenerative therapy2021

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

Masaaki Yano, Alessandro Nasti, Akihiro Seki, Kosuke Ishida, Masatoshi Yamato, Hiiro Inui, Norihiko Ogawa, Shingo Inagaki, Tuyen Thuy Bich Ho, Kazunori Kawaguchi and 12 more

Open access · goldAbstract read
In one paragraph

Article in Regenerative therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 8 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors at 2 institutions in 1 country.

Masaaki YanoDepartment of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Alessandro NastiSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.
Akihiro SekiDepartment of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.
Kosuke IshidaSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.
Masatoshi YamatoDepartment of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Hiiro InuiDepartment of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Norihiko OgawaSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.
Shingo InagakiSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.
Tuyen Thuy Bich HoSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Kanazawa, Japan.
Kazunori KawaguchiDepartment of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.
Taro YamashitaDepartment of General Medicine, Kanazawa University Hospital, Kanazawa, Japan.
Kuniaki AraiDepartment of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.
Tatsuya YamashitaDepartment of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.
Eishiro MizukoshiDepartment of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.
Oto InoueDepartment of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.
Shinichiro TakashimaDepartment of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.
Soichiro UsuiDepartment of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.
Masayuki TakamuraDepartment of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Japan.
Masao HondaDepartment of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.
Takashi WadaDepartment of Nephrology and Laboratory Medicine, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Shuichi KanekoDepartment of Gastroenterology, Graduate School of Medical Sciences, Kanazawa University, Kanazawa, Japan.
Yoshio SakaiDepartment of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan.
Kanazawa University Hospital · JPKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionFreshly 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).

methodsThe 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.

resultsWild-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.

conclusionsNASH-derived u-ADSCs, similar to wild-type u-ADSCs, are applicable for reparative and regenerative therapy in mice with NASH.

Indexed as

Adipose tissueAST, aspartate aminotransferaseAT-HF, atherogenic high-fatFCM, flow cytometryHICs, hepatic inflammatory cellsLD, lactate dehydrogenaseMesenchymal stem cellsMSCs, mesenchymal stem cellsNAFLD, nonalcoholic fatty liver diseaseNASH (12 w) u-ADSCs, NASH (12 weeks)-derived u-ADSCsNASH (4w) u-ADSCs, NASH (4 weeks)-derived u-ADSCsNASH, nonalcoholic steatohepatitisNAS, NAFLD activity scoreNon-alcoholic fatty liver diseaseqRT-PCR, quantitative real-time polymerase chain reactionStromal cellsu-ADSCs, uncultured adipose tissue-derived stromal cells

Identifiers

PMID34926735
PMCPMC8649123
OpenAlexW4200312335

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.