Evidence map›Paper›PMID 27748901›Full record

ArticleMolecular medicine reports2016

Screening of differentially expressed protein kinases in bone marrow endothelial cells and the protective effects of the p38a inhibitor SB203580 on bone marrow in liver fibrosis.

Bo Gao, Wang Sun, Xianzhi Meng, Dongbo Xue, Weihui Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 83% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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 2 institutions in 1 country.

Bo GaoDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Wang SunDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Xianzhi MengDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Dongbo XueDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Weihui ZhangDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematological abnormalities are frequently observed in patients with liver cirrhosis (LC). A previous study demonstrated that the apoptosis and damage of endothelial cells could cause the hematological abnormalities in LC. Protein kinases are one of the most important factors that regulate cell behavior, and are potential therapeutic targets for the treatment of a number of diseases. In a previous study, whole genome profiling was used to identify differentially expressed genes in human bone marrow endothelial cells treated with serum from 26 patients with LC. From this data set, the present study identified 14 differentially expressed kinase genes in human bone marrow endothelial cells in LC from the microarray data, including p38a, AKT1 and PDK1. Pathway analysis revealed that these kinase genes were enriched in certain important LC‑associated pathways (e.g. MAPK and WNT signaling pathway). Literature mining revealed that p38a was associated with bone marrow apoptosis; therefore, p38a and its inhibitor, SB203580, were selected as potential therapeutic targets in the present study. The results of hematoxylin‑eosin and Masson's trichrome staining of livers from a rat model of liver fibrosis (LF) that underwent ligation of the bile duct demonstrated that SB203580 reduced the degree of LF. In addition, SB203580‑treated rats with LF demonstrated a significantly higher number of platelets when compared with the untreated group. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis indicated that apoptosis of bone marrow tissue in rats with LF was inhibited by SB203580. In addition, the results from the immunohistochemical analysis demonstrated that SB203580 reduced the expression of von Willebrand factor and caspase 3 in the bone marrow of rats with LF. In conclusion, the results from the present study indicate that the p38a kinase inhibitor, SB203580, may exhibit a protective effect on bone marrow tissues in rats with LF. This suggests that protein kinases and their inhibitors may present novel therapeutic strategies for the treatment of hematological abnormalities in patients with LC.

Indexed as

AnimalsApoptosisBlood PlateletsBone Marrow CellsDisease Models, AnimalEndothelial CellsGene Expression RegulationHematologic DiseasesHumansImidazolesLiver Cirrhosisp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyridinesImidazolesp38 Mitogen-Activated Protein KinasesPDK1 protein, humanPdk1 protein, ratProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyridinesPyruvate Dehydrogenase Acetyl-Transferring KinaseSB 203580

Identifiers

PMID27748901
PMCPMC5102023
OpenAlexW2530534490

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.