Evidence map›Paper›PMID 24130040›Full record

ArticleMolecular and cellular biochemistry2014

Wnt/β-catenin signaling mediates the senescence of bone marrow-mesenchymal stem cells from systemic lupus erythematosus patients through the p53/p21 pathway.

Zhifeng Gu, Wei Tan, Guijuan Feng, Yan Meng, Biyu Shen, Hong Liu, Chun Cheng

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 85 citations in OpenAlex.

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  16. Vangl2 Promotes Hematopoietic Stem Cell Expansion.Frontiers in cell and developmental biology · 2022
    Article
  17. A Small-Molecule Cocktails-Based Strategy in Culture of Mesenchymal Stem Cells.Frontiers in bioengineering and biotechnology · 2022
    Article
  18. Review
  19. Review
  20. Citrus Alkaline Extracts Inhibit Senescence of A549 Cells to Alleviate Pulmonary Fibrosis via the β-Catenin/P53 Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2021
    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

7 authors at 2 institutions in 1 country.

Zhifeng GuDepartment of Rheumatology, Affiliated Hospital of Nantong University, Nantong, China, guzhifeng@126.com.
Wei Tan
Guijuan Feng
Yan Meng
Biyu Shen
Hong Liu
Chun Cheng
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that allogeneic bone marrow (BM)-mesenchymal stem cell transplantation (MSCT) appears to be effective in systemic lupus erythematosus (SLE) patients and lupus-prone mice, contrary to studies in syngeneic BM-MSCT. These studies indicated that the abnormalities of BM-MSCs may be involved in the pathogenesis of SLE. Our studies and other previous studies have revealed that BM-MSCs from SLE patients exhibited early signs of senescence, such as flattened morphology, slow proliferation, increased senescence-associated β-galactosidase (SA-β-gal) activity, and so on. However, the mechanisms by which these cells senescences were still unclear. Previous studies have demonstrated that Wnt/β-catenin signaling plays an important role in stem cell senescence. In the current study, we investigated whether Wnt/β-catenin signaling mediates the senescence of BM-MSCs from SLE patients. We have found that Wnt/β-catenin signaling and the p53/p21 pathway were significantly hyperactivated in senescent SLE BM-MSCs. Treatment with 100 ng/mL Dickkopf-1 (DKK1), a Wnt/β-catenin signaling inhibitor or β-catenin siRNA for 48 h could reverse the senescent features of SLE BM-MSCs. Additionally, the expression levels of p53 and p21 were reduced in treated-SLE BM-MSCs compared with the untreated group. In summary, our study indicated that Wnt/β-catenin signaling may play a critical role in the senescence of SLE BM-MSCs through the p53/p21 pathway.

Indexed as

Cellular SenescenceWnt Signaling PathwayAdolescentAdultbeta CateninBone Marrow CellsCase-Control StudiesCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21FemaleHumansIntercellular Signaling Peptides and ProteinsLupus Erythematosus, SystemicMesenchymal Stem CellsTumor Suppressor Protein p53beta CateninCDKN1A protein, humanCTNNB1 protein, humanCyclin-Dependent Kinase Inhibitor p21DKK1 protein, humanIntercellular Signaling Peptides and ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24130040
OpenAlexW2090734635

What OpenQuestion holds

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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.