Evidence map›Paper›PMID 25661318›Full record

ArticleActa pharmacologica Sinica2015

GSK-3β suppresses the proliferation of rat hepatic oval cells through modulating Wnt/β-catenin signaling pathway.

Xiao-ke Ji, Yuan-kang Xie, Jun-qiao Zhong, Qi-gang Xu, Qi-qiang Zeng, Yang Wang, Qi-yu Zhang, Yun-feng Shan

Abstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Wnt-β-catenin signalling in liver development, health and disease.Nature reviews. Gastroenterology & hepatology · 2019
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. GSK-3β as a target for protection against transient cerebral ischemia.International journal of medical sciences · 2017
    Article
  10. Article
  11. Article
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.

Xiao-ke JiDepartment of General Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Yuan-kang XieDepartment of General Surgery, the First Affiliated Hospital of Gannan Medical College, Ganzhou 341000, China.
Jun-qiao ZhongDepartment of General Surgery, Ganzhou People's Hospital, Ganzhou 341000, China.
Qi-gang XuDepartment of General Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Qi-qiang ZengDepartment of General Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Yang WangDepartment of General Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Qi-yu ZhangDepartment of General Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.
Yun-feng ShanDepartment of General Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimGlycogen synthase kinase 3β (GSK-3β) plays a crucial role in hepatic biology, including liver development, regeneration, proliferation and carcinogenesis. In this study we investigated the role of GSK-3β in regulation of growth of hepatic oval cells in vitro and in liver regeneration in partially hepatectomized rats.

methodsWB-F344 cells, the rat hepatic stem-like epithelial cells, were used as representative of oval cells. Cell viability was examined using a WST-8 assay. The cells were transfected with a recombinant lentivirus expressing siRNA against GSK-3β (GSK-3βRNAiLV) or a lentivirus that overexpressed GSK-3β (GC-GSK-3βLV). Adult rats underwent partial (70%) hepatectomy, and liver weight and femur length were measured at d 7 after the surgery. The expression of GSK-3β, phospho-Ser9-GSK-3β, β-catenin and cyclin D1 was examined with immunoblotting assays or immunohistochemistry.

resultsTreatment of WB-F344 cells with the GSK-3β inhibitor SB216763 (5 and 10 μmol/L) dose-dependently increased the levels of phospho-Ser9-GSK-3β, but not the levels of total GSK-3β, and promoted the cell proliferation. Knockout of GSK-3β with GSK-3βRNAiLV increased the cell proliferation, whereas overexpression of GSK-3β with GC-GSK-3βLV decreased the proliferation. Both SB216763 and GSK-3βRNAiLV significantly increased the levels of β-catenin and cyclin D1 in the cells, whereas GSK-3β overexpression decreased their levels. In rats with a partial hepatectomy, administration of SB216763 (2 mg/kg, ip) significantly increased the number of oval cells, the levels of phospho-Ser9-GSK-3β, β-catenin and cyclin D1 in liver, as well as the ratio of liver weight to femur length at d 7 after the surgery.

conclusionGSK-3β suppresses the proliferation of hepatic oval cells by modulating the Wnt/β-catenin signaling pathway.

Indexed as

Cell ProliferationLiver RegenerationWnt Signaling PathwayAnimalsbeta CateninCyclin D1Epithelial CellsGene Expression Regulation, EnzymologicGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHEK293 CellsHepatectomyHumansLiverMaleOrgan Sizebeta CateninCcnd1 protein, ratCtnnb1 protein, ratCyclin D1Glycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, ratProtein Kinase Inhibitors

Identifiers

PMID25661318
PMCPMC4349928

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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.