Evidence map›Paper›PMID 26722604›Full record

ArticleInternational journal of clinical and experimental pathology2015

Effect of p38 mitogen-activate protein kinase on MUC5AC protein expression of bile duct epithelial cells in hepatolithiasis patients.

Ping Wang, Xiaodong Ma, Yu He, Beiwang Sun, Canhua Zhu, Rujin Zhao, Shaoling Zhang, Xianxian Huang, Yanmin Liu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. 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

9 authors at 3 institutions in 1 country.

Ping WangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangzhou Medical University Guangzhou, Guangdong, P.R. China.
Xiaodong MaInstitute of Materia Medica, South China Normal University Guangzhou, Guangdong, P.R. China.
Yu HeDepartment of Hepatobiliary Surgery, Southwest Hospital, Third Military University Chongqing, P.R. China.
Beiwang SunDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangzhou Medical University Guangzhou, Guangdong, P.R. China.
Canhua ZhuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangzhou Medical University Guangzhou, Guangdong, P.R. China.
Rujin ZhaoDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangzhou Medical University Guangzhou, Guangdong, P.R. China.
Shaoling ZhangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangzhou Medical University Guangzhou, Guangdong, P.R. China.
Xianxian HuangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangzhou Medical University Guangzhou, Guangdong, P.R. China.
Yanmin LiuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangzhou Medical University Guangzhou, Guangdong, P.R. China.
First Affiliated Hospital of Guangzhou Medical University · CNSouth China Normal University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary hepatolithiasis is a common bile duct disease with benign nature but complicated mechanisms. Current studies have revealed its correlation with cytokine release by chronic inflammation, which also increased mucin (MUC) synthesis. This study investigated the role of p38 mitogen-activated protein kinase (MAPK) in regulating cytokine release and mucin synthesis, in an attempt to elucidate the role of p38 signaling molecule in the pathogenesis of hepatolithiasis. In human intrahepatic bile duct endothelial cells (HIBECs), lipoprotein (LPS) was used to induce the high expression of MUC. Small interference RNA (siRNA) was then used to silencing p38 gene expression. Cytokines including interleukin (IL)-1β and tumor necrosis factor (TNF)-α were measured, along with MUC5AC protein and mRNA expression assay. The interference of p38 gene expression inhibited the release of IL-1β and TNF-α in cultured cells. It also depressed both mRNA and protein levels of MUC5A. P38 MAPK signal pathway may be involved in the formation and progression of hepatolithiasis. This study provides potential new strategy for treating hepatolithiasis using p38 MAPK signal pathway as the drug target.

Indexed as

Gene Expression RegulationMAP Kinase Signaling SystemBile Duct DiseasesBile Ducts, IntrahepaticCells, CulturedCytokinesEpithelial CellsHumansInterleukin-1betaMucin 5ACp38 Mitogen-Activated Protein KinasesPhosphorylationRNA, MessengerRNA, Small InterferingTumor Necrosis Factor-alphaCytokinesInterleukin-1betaMUC5AC protein, humanMucin 5ACp38 Mitogen-Activated Protein KinasesRNA, MessengerRNA, Small InterferingTumor Necrosis Factor-alphaHepatolithiasislipoproteinmucinp38 MAPK

Identifiers

PMID26722604
PMCPMC4680549
OpenAlexW2418290313

What OpenQuestion holds

Textmetadata
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.