Evidence map›Paper›PMID 35379781›Full record

ArticleCell death & disease2022

GITR/GITRL reverse signalling modulates the proliferation of hepatic progenitor cells by recruiting ANXA2 to phosphorylate ERK1/2 and Akt.

Yu He, Yufeng Pei, Kai Liu, Lin Liu, Yue Tian, Hongyi Li, Min Cong, Tianhui Liu, Hong Ma, Hong You and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

13 authors at 2 institutions in 1 country.

Yu He *Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Yufeng Pei *Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Kai Liu *Beijing Clinical Research Institute, Beijing, China.
Lin LiuLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Yue TianBeijing Clinical Research Institute, Beijing, China.
Hongyi LiLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Min CongLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Tianhui LiuLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Hong MaLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Hong YouLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Jidong JiaLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China. jia_jd@ccmu.edu.cn.
Dong ZhangBeijing Clinical Research Institute, Beijing, China. zhangd@ccmu.edu.cn.
Ping WangLiver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing, China. wangping2009@ccmu.edu.cn.ORCID 0000-0002-1395-2014
Capital Medical University · CNBeijing University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic stem/progenitor cells are the major cell compartment for tissue repair when hepatocyte proliferation is compromised in chronic liver diseases, but the expansion of these cells increases the risk of carcinogenesis. Therefore, it is essential to explore the pathways restricting their expansion and abnormal transformation. The ligand of glucocorticoid-induced tumour necrosis factor receptor (GITRL) showed the most highly increased expression in hepatic progenitor cells treated with transforming growth factor (TGF)-β1. If overexpressed by hepatic progenitor cells, GITRL stimulated cell proliferation by activating the epithelial-mesenchymal transition pathway and enhancing ERK1/2 and Akt phosphorylation via GITRL binding to ANXA2. However, GITR, the specific GITRL receptor, suppressed the epithelial-mesenchymal transition pathway of GITRL-expressing cells and decreased their growth by dissociating ANXA2 from GITRL and reducing downstream ERK1/2 and Akt phosphorylation. This study identifies GITR/GITRL reverse signalling as a cross-interaction pathway between immune cells and hepatic stem/progenitor cells that restricts the expansion of hepatic stem/progenitor cells and reduces the possibility of carcinogenesis.

Indexed as

Annexin A2Tumor Necrosis FactorsCarcinogenesisCell ProliferationGlucocorticoid-Induced TNFR-Related ProteinHumansMAP Kinase Signaling SystemProto-Oncogene Proteins c-aktStem CellsAnnexin A2ANXA2 protein, humanGlucocorticoid-Induced TNFR-Related ProteinProto-Oncogene Proteins c-aktTumor Necrosis Factors

Identifiers

PMID35379781
PMCPMC8979965
OpenAlexW4223533362

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.