Evidence map›Paper›PMID 27956229›Full record

ArticleGastroenterology2017

Milk Fat Globule-EGF Factor 8, Secreted by Mesenchymal Stem Cells, Protects Against Liver Fibrosis in Mice.

Su Yeon An, Yu Jin Jang, Hee-Joung Lim, Jiyou Han, Jaehun Lee, Gyunggyu Lee, Ji Young Park, Seo-Young Park, Ji Hyang Kim, Byung-Rok Do and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 4% 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

110 citing papers in PubMed, 2 syntheses or guidelines pooled it, 213 citations in OpenAlex.

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  18. Extracellular vesicles: emerging therapeutic agents for liver fibrosis.Extracellular vesicles and circulating nucleic acids · 2025
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50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 1 country.

Su Yeon AnLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Yu Jin JangLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Hee-Joung LimLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Jiyou HanLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Jaehun LeeLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Gyunggyu LeeLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Ji Young ParkLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Seo-Young ParkLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
Ji Hyang KimBiotechnology Research Institute, HurimBioCell Inc., Seoul, Republic of Korea.
Byung-Rok DoBiotechnology Research Institute, HurimBioCell Inc., Seoul, Republic of Korea.
Choongseong HanDepartment of Oral Medicine and Oral Diagnosis, Seoul National University Dental Hospital, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Republic of Korea; Nexel, Co., Ltd, Seoul, Republic of Korea.
Hee-Kyung ParkDepartment of Oral Medicine and Oral Diagnosis, Seoul National University Dental Hospital, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Republic of Korea.
Ok-Hee KimDepartment of Surgery, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Daejeon, Republic of Korea.
Myeong Jun SongDivision of Hepatology, Department of Internal Medicine, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Daejeon, Republic of Korea.
Say-June KimDepartment of Surgery, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Daejeon, Republic of Korea.
Jong-Hoon KimLaboratory of Stem Cells and Tissue Regeneration, Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea. Electronic address: jhkim@korea.ac.kr.
Korea University · KRKorea Research Institute of Bioscience and Biotechnology · KRThe Catholic University of Korea Daejeon St. Mary's Hospital · KRCatholic University of Korea · KRGS Caltex (South Korea) · KRSeoul National University Dental Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsMesenchymal stem cells (MSCs) mediate tissue repair and might be used to prevent or reduce liver fibrosis. However, little is known about the anti-fibrotic factors secreted from MSCs or their mechanisms.

methodsUmbilical cord-derived MSCs (UCMSCs) were differentiated into hepatocyte-like cells (hpUCMSCs), medium was collected, and secretome proteins were identified and quantified using nanochip-liquid chromatography/quadrupole time-of-flight mass spectrometry. Liver fibrosis was induced in mice by intraperitoneal injection of thioacetamide or CCl

resultsIn mice with fibrosis, accumulation of extracellular matrix proteins was significantly reduced 3 days after injecting secretomes from UCMSCs, and to a greater extent from hpUCMSCs; numbers of activated HSCs that expressed the myogenic marker α-smooth muscle actin (α-SMA, encoded by ACTA2 [actin, alpha 2, smooth muscle]) were also reduced. Secretomes from UCMSCs, and to a greater extent from hpUCMSCs, reduced liver expression of multiple fibrotic factors, collagens, metalloproteinases, TGFβ, and Smad proteins in the TGFβ signaling pathways. In HSC cell lines and primary HSCs, TGFβ1-stimulated upregulation of α-SMA was significantly inhibited (and SMAD2 phosphorylation reduced) by secretomes from UCMSCs, and to a greater extent from hpUCMSCs. We identified 32 proteins in secretomes of UCMSCs that were more highly concentrated in secretomes from hpUCMSCs and inhibited TGFβ-mediated activation of HSCs. One of these, milk fat globule-EGF factor 8 (MFGE8), was a strong inhibitor of activation of human primary HSCs. We found MFGE8 to down-regulate expression of TGFβ type I receptor by binding to α

conclusionsMFGE8 is an anti-fibrotic protein in MSC secretomes that strongly inhibits TGFβ signaling and reduces extracellular matrix deposition and liver fibrosis in mice.

Indexed as

AnimalsAntigens, SurfaceCarbon TetrachlorideCell LineCollagenExtracellular MatrixHepatic Stellate CellsHepatocytesHumansIntegrin alphaVbeta3Liver CirrhosisMaleMesenchymal Stem CellsMetabolomeMetalloproteasesMiceAntigens, SurfaceCarbon TetrachlorideCollagenIntegrin alphaVbeta3MetalloproteasesMFGE8 protein, humanMfge8 protein, mouseMilk ProteinsReceptors, Transforming Growth Factor betaSmad2 ProteinTGFB1 protein, humanTgfb1 protein, mouseThioacetamideTransforming Growth Factor beta1DecorinMMPMouse ModelSignal Transduction

Identifiers

PMID27956229
OpenAlexW2560581251

What OpenQuestion holds

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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.