Evidence map›Paper›PMID 25889917›Full record

ArticleStem cell research & therapy2015

Systematic implantation of dedifferentiated fat cells ameliorated monoclonal antibody 1-22-3-induced glomerulonephritis by immunosuppression with increases in TNF-stimulated gene 6.

Takashi Maruyama, Noboru Fukuda, Taro Matsumoto, Koichiro Kano, Morito Endo, Minako Kazama, Tomohiko Kazama, Jin Ikeda, Hiroyuki Matsuda, Takahiro Ueno and 5 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 20 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

15 authors at 3 institutions in 1 country.

Takashi MaruyamaDivision of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. maruyama.takashi@nihon-u.ac.jp.
Noboru FukudaDivision of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. fukuda.noboru@nihon-u.ac.jp.
Taro MatsumotoDivision of Cell Regeneration and Transplantation, Department of Functional Morphology, Nihon University School of Medicine, Tokyo, Japan. matsumoto.taro@nihon-u.ac.jp.
Koichiro KanoLaboratory of Cell and Tissue Biology, College of Bioresource Science, Nihon University, Fujisawa, Japan. kano.kouichirou@nihon-u.ac.jp.
Morito EndoFaculty of Human Health Science, Hachinohe Gakuin University, Hachinohe, Aomori, Japan. mendo@htv-net.ne.jp.
Minako KazamaDepartment of Pediatrics, Nihon University School of Medicine, Tokyo, Japan. fwnz2459@mb.infoweb.ne.jp.
Tomohiko KazamaDivision of Cell Regeneration and Transplantation, Department of Functional Morphology, Nihon University School of Medicine, Tokyo, Japan. kazama.tomohiko@nihon-u.ac.jp.
Jin IkedaDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. septembre.99@gmail.com.
Hiroyuki MatsudaDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. hiroyuki.matsuda@med.nihon-u.ac.jp.
Takahiro UenoDivision of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. ueno.takahiro@nihon-u.ac.jp.
Masanori AbeDivision of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. abe.masanori@nihon-u.ac.jp.
Kazuyoshi OkadaDivision of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. okada.kazuyoshi@nihon-u.ac.jp.
Masayoshi SomaDivision of General Medicine, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. souma.masayoshi@nihon-u.ac.jp.
Koichi MatsumotoDivision of Nephrology Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. matsumoto.koichi91@nihon-u.ac.jp.
Hiroshi KawachiDepartment of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. kawachi@med.niigata-u.ac.jp.
Nihon University · JPHachinohe Gakuin University · JPNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionImplantation of mesenchymal stem cells (MSCs) has recently been reported to repair tissue injuries through anti-inflammatory and immunosuppressive effects. We established dedifferentiated fat (DFAT) cells that show identical characteristics to MSCs.

methodsWe examined the effects of 10(6) of DFAT cells infused through renal artery or tail vein on monoclonal antibody (mAb) 1-22-3-induced glomerulonephritis (as an immunological type of renal injury) and adriamycin-induced nephropathy (as a non-immunological type of renal injury) in rats. The mAb 1-22-3-injected rats were also implanted with 10(6) of DFAT cells transfected with TSG-6 siRNA through tail vein.

resultsAlthough DFAT cells transfused into blood circulation through the tail vein were trapped mainly in lungs without reaching the kidneys, implantation of DFAT cells reduced proteinuria and improved glomerulosclerosis and interstitial fibrosis. Implantation of DFAT cells through the tail vein significantly decreased expression of kidney injury molecule-1, collagen IV and fibronectin mRNAs, whereas nephrin mRNA expression was increased. Implantation of DFAT cells did not improve adriamycin-induced nephropathy, but significantly decreased the glomerular influx of macrophages, common leukocytes and pan T cells. However, the glomerular influx of helper T cells, was increased. Implantation of DFAT cells decreased expression of interleukin (IL)-6 and IL-12β mRNAs and increased expression of TNF-stimulated gene (TSG)-6 mRNA in renal cortex from mAb 1-22-3-injected rats. The basal level of TSG-6 protein was significantly higher in DFAT cells than in fibroblasts. Expression of TSG-6 mRNA in MCs cocultured with DFAT cells was significantly higher than in mesangial cells or DFAT cells alone. Systematic implantation of DFAT cells with TSG-6 siRNA through tail vein did not improve proteinuria, renal dysfunction and renal degeneration in the mAb 1-22-3-injected rats.

conclusionSystematic implantation of DFAT cells effectively ameliorated mAb 1-22-3-induced glomerulonephritis through immunosuppressive effects accompanied by the suppression of macrophage infiltration and expression of IL-6, IL-10 and IL-12β, and increased production of serum and renal TSG-6 that improved the mAb 1-22-3-induced renal degeneration by the immunosuppressive effects of TSG-6. Thus DFAT cells will be suitable cell source for the treatment of immunological progressive renal diseases.

Indexed as

Stem Cell TransplantationAdipose TissueAnimalsAntibodies, MonoclonalCell Adhesion MoleculesCell DedifferentiationCoculture TechniquesCytokinesGlomerulonephritisImmunosuppression TherapyKidney CortexMacrophagesMaleMiceMice, Inbred BALB CNephritisAntibodies, MonoclonalCell Adhesion MoleculesCytokinesTnfaip6 protein, rat

Identifiers

PMID25889917
PMCPMC4455708
OpenAlexW2137451247

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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.