Evidence map›Paper›PMID 25145391›Full record

ArticleExperimental & molecular medicine2014

Therapeutic effect of hepatocyte growth factor-secreting mesenchymal stem cells in a rat model of liver fibrosis.

Myung-Deok Kim, Sung-Soo Kim, Hyun-Young Cha, Seung-Hun Jang, Da-Young Chang, Wookhwan Kim, Haeyoung Suh-Kim, Jae-Ho Lee

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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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

8 authors.

Myung-Deok Kim1] Department of Biochemistry, Ajou University School of Medicine, Suwon, Republic of Korea [2] Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon, Republic of Korea.
Sung-Soo Kim1] Department of Anatomy, Ajou University School of Medicine, Suwon, Republic of Korea [2] Center for Cell Death Regulating Biodrug, Ajou University School of Medicine, Suwon, Republic of Korea.
Hyun-Young ChaDepartment of Biochemistry, Ajou University School of Medicine, Suwon, Republic of Korea.
Seung-Hun Jang1] Department of Biochemistry, Ajou University School of Medicine, Suwon, Republic of Korea [2] Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon, Republic of Korea.
Da-Young ChangDepartment of Anatomy, Ajou University School of Medicine, Suwon, Republic of Korea.
Wookhwan Kim1] Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon, Republic of Korea [2] Department of General Surgery, Ajou University School of Medicine, Suwon, Republic of Korea.
Haeyoung Suh-KimDepartment of Anatomy, Ajou University School of Medicine, Suwon, Republic of Korea.
Jae-Ho Lee1] Department of Biochemistry, Ajou University School of Medicine, Suwon, Republic of Korea [2] Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow-derived mesenchymal stromal cells (MSCs) have been reported to be beneficial for the treatment of liver fibrosis. Here, we investigated the use of genetically engineered MSCs that overexpress hepatocyte growth factor (HGF) as a means to improve their therapeutic effect in liver fibrosis. Liver fibrosis was induced by intraperitoneal injection of dimethylnitrosamine. HGF-secreting MSCs (MSCs/HGF) were prepared by transducing MSCs with an adenovirus carrying HGF-encoding cDNA. MSCs or MSCs/HGF were injected directly into the spleen of fibrotic rats. Tissue fibrosis was assessed by histological analysis 12 days after stem cell injection. Although treatment with MSCs reduced fibrosis, treatment with MSCs/HGF produced a more significant reduction and was associated with elevated HGF levels in the portal vein. Collagen levels in the liver extract were decreased after MSC/HGF therapy, suggesting recovery from fibrosis. Furthermore, liver function was improved in animals receiving MSCs/HGF, indicating that MSC/HGF therapy resulted not only in reduction of liver fibrosis but also in improvement of hepatocyte function. Assessment of cell and biochemical parameters revealed that mRNA levels of the fibrogenic cytokines PDGF-bb and TGF-β1 were significantly decreased after MSC/HGF therapy. Subsequent to the decrease in collagen, expression of matrix metalloprotease-9 (MMP-9), MMP-13, MMP-14 and urokinase-type plasminogen activator was augmented following MSC/HGF, whereas tissue inhibitor of metalloprotease-1 (TIMP-1) expression was reduced. In conclusion, therapy with MSCs/HGF resulted in an improved therapeutic effect compared with MSCs alone, probably because of the anti-fibrotic activity of HGF. Thus, MSC/HGF represents a promising approach toward a cell therapy for liver fibrosis.

Indexed as

Genetic EngineeringMesenchymal Stem Cell TransplantationUp-RegulationAnimalsCell EngineeringCells, CulturedHepatocyte Growth FactorHumansLiverLiver CirrhosisMaleMesenchymal Stem CellsRatsRats, Sprague-DawleyHepatocyte Growth Factor

Identifiers

PMID25145391
PMCPMC4150933

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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.