Evidence map›Paper›PMID 28623272›Full record

ArticleScientific reports2017

Exosomes derived from palmitic acid-treated hepatocytes induce fibrotic activation of hepatic stellate cells.

Young-Sun Lee, So Yeon Kim, Eunjung Ko, Jun-Hee Lee, Hyon-Seung Yi, Yang Jae Yoo, Jihye Je, Sang Jun Suh, Young Kul Jung, Ji Hoon Kim and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 2 pooled it
10.5field-weighted citation impact, top 1% 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

141 citing papers in PubMed, 2 syntheses or guidelines pooled it, 236 citations in OpenAlex.

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81 more citing papers are in PubMed but not listed here.

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

16 authors at 3 institutions in 2 countries.

Young-Sun LeeDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.ORCID 0000-0001-6396-0859
So Yeon KimLab of Liver Research, Biomedical Science and Engineering Interdisciplinary Program, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea.ORCID 0000-0003-1319-6164
Eunjung KoDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Jun-Hee LeeGraduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea.
Hyon-Seung YiDepartment of Internal Medicine, Chungnam National University School of Medicine, Daejeon, 305-764, Republic of Korea.
Yang Jae YooDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Jihye JeDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Sang Jun SuhDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Young Kul JungDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Ji Hoon KimDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Yeon Seok SeoDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Hyung Joon YimDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Won-Il JeongLab of Liver Research, Biomedical Science and Engineering Interdisciplinary Program, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 34141, Republic of Korea.
Jong Eun YeonDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea. jeyyeon@hotmail.com.
Soon Ho UmDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Kwan Soo ByunDepartment of Internal Medicine, Korea University College of Medicine, Seoul, Korea.
Korea University · KRKorea Advanced Institute of Science and Technology · KRChungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a dominant cause of chronic liver disease, but the exact mechanism of progression from simple steatosis to nonalcoholic steatohepatitis (NASH) remains unknown. Here, we investigated the role of exosomes in NAFLD progression. Exosomes were isolated from a human hepatoma cell line treated with palmitic acid (PA) and their miRNA profiles examined by microarray. The human hepatic stellate cell (HSC) line (LX-2) was then treated with exosome isolated from hepatocytes. Compared with controls, PA-treated hepatocytes displayed significantly increased CD36 and exosome production. The microarray analysis showed there to be distinctive miRNA expression patterns between exosomes from vehicle- and PA-treated hepatocytes. When LX-2 cells were cultured with exosomes from PA-treated hepatocytes, the expression of genes related to the development of fibrosis were significantly amplified compared to those treated with exosomes from vehicle-treated hepatocytes. In conclusion, PA treatment enhanced the production of exosomes in these hepatocytes and changed their exosomal miRNA profile. Moreover, exosomes derived from PA-treated hepatocytes caused an increase in the expression levels of fibrotic genes in HSCs. Therefore, exosomes may have important roles in the crosstalk between hepatocytes and HSCs in the progression from simple steatosis to NASH.

Indexed as

AnimalsCell Line, TumorExosomesGene Expression ProfilingHepatic Stellate CellsHepatocytesHumansLiver CirrhosisMaleMiceMicroRNAsPalmitic AcidTranscriptomeMicroRNAsPalmitic Acid

Identifiers

PMID28623272
PMCPMC5473841
OpenAlexW2625576839

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.