Evidence map›Paper›PMID 27729629›Full record

ArticleClinical and molecular hepatology2016

Decreased C-reactive protein induces abnormal vascular structure in a rat model of liver dysfunction induced by bile duct ligation.

Ji Hye Jun, Jong Ho Choi, Si Hyun Bae, Seh Hoon Oh, Gi Jin Kim

Open access · goldAbstract read
In one paragraph

Article in Clinical and molecular hepatology, 2016. 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
0.5field-weighted citation impact, top 29% 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, 11 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

5 authors at 3 institutions in 2 countries.

Ji Hye JunDepartment of Biomedical Science, CHA University, Seongnam, Korea.
Jong Ho ChoiDepartment of Biomedical Science, CHA University, Seongnam, Korea.
Si Hyun BaeDepartment of Internal Medicine, Catholic University Medical College, Seoul, Korea.
Seh Hoon OhDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida, College of Medicine, Gainsville, FL, USA.
Gi Jin KimDepartment of Biomedical Science, CHA University, Seongnam, Korea.
CHA University · KRCatholic University of Korea · KRFlorida College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsChronic liver disease leads to liver fibrosis, and although the liver does have a certain regenerative capacity, this disease is associated with dysfunction of the liver vessels. C-reactive protein (CRP) is produced in the liver and circulated from there for metabolism. CRP was recently shown to inhibit angiogenesis by inducing endothelial cell dysfunction. The objective of this study was to determine the effect of CRP levels on angiogenesis in a rat model of liver dysfunction induced by bile duct ligation (BDL).

methodsThe diameter of the hepatic vein was analyzed in rat liver tissues using hematoxylin and eosin (H&E) staining. The expression levels of angiogenic factors, albumin, and CRP were analyzed by real-time PCR and Western blotting. A tube formation assay was performed to confirm the effect of CRP on angiogenesis in human umbilical vein endothelial cells (HUVECs) treated with lithocholic acid (LCA) and siRNA-CRP.

resultsThe diameter of the hepatic portal vein increased significantly with the progression of cirrhosis. The expression levels of angiogenic factors were increased in the cirrhotic liver. In contrast, the expression levels of albumin and CRP were significantly lower in the liver tissue obtained from the BDL rat model than in the normal liver. The CRP level was correlated with the expression of albumin in hepatocytes treated with LCA and siRNA-CRP. Tube formation was significantly decreased in HUVECs when they were treated with LCA or a combination of LCA and siRNA-CRP.

conclusionCRP seems to be involved in the abnormal formation of vessels in hepatic disease, and so it could be a useful diagnostic marker for hepatic disease.

Indexed as

Angiogenic ProteinsAnimalsBile DuctsCells, CulturedC-Reactive ProteinDisease Models, AnimalHepatic VeinsHepatocytesHumansHuman Umbilical Vein Endothelial CellsLithocholic AcidLiverLiver CirrhosisLiver DiseasesMaleMicroscopy, FluorescenceAngiogenic ProteinsC-Reactive ProteinLithocholic AcidRNA, Small InterferingSerum AlbuminBile duct ligationC-reactive proteinHepatic diseasePrimary biliary cirrhosis

Identifiers

PMID27729629
PMCPMC5066379
OpenAlexW2524294898

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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.