Evidence map›Paper›PMID 31831024›Full record

ArticleJournal of orthopaedic surgery and research2019

The regulatory mechanism of p38/MAPK in the chondrogenic differentiation from bone marrow mesenchymal stem cells.

Ning Ma, Xiao Teng, Qi Zheng, Peng Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of orthopaedic surgery and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.9field-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

37 citing papers in PubMed, 55 citations in OpenAlex.

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  10. Research progress and prospect of MAPK signaling pathway in knee osteoarthritis.European journal of orthopaedic surgery & traumatology : orthopedie traumatologie · 2025
    Review
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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

4 authors at 2 institutions in 1 country.

Ning MaDepartment of Orthopedics, Zhejiang Taizhou Central Hospital (Affiliated Hospital of Taizhou University), No. 999 Donghai Avenue, Jiaojiang District, Taizhou, 318000, Zhejiang, China.
Xiao TengDepartment of Orthopedics, Zhejiang Taizhou Central Hospital (Affiliated Hospital of Taizhou University), No. 999 Donghai Avenue, Jiaojiang District, Taizhou, 318000, Zhejiang, China.
Qi ZhengDepartment of Orthopedics, Zhejiang Taizhou Central Hospital (Affiliated Hospital of Taizhou University), No. 999 Donghai Avenue, Jiaojiang District, Taizhou, 318000, Zhejiang, China.
Peng ChenDepartment of Orthopedics, Yan Cheng Third People's Hospital (Affiliated Yancheng Hospital of Southeast University Medical College), No.2 Xindu West Road, Yancheng, 224001, Jiangsu, China. doctorchen51@163.com.
Taizhou University · CNYancheng Third People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation and joint inflammation, in which growth factors are significantly involved. The extracellular signal-regulated p38 MAPK pathways play important roles in the regulation of osteogenic and chondrogenic differentiation in bone marrow mesenchymal stem cells (BMSCs). However, the exact mechanism remains unclear.

methodsIn this study, the chondrogenic differentiation of human BMSCs was initiated in micromass culture in the presence of TGF-β1 for 14 days. Quantitative RT-PCR and Western blot were performed to detect the transfection effect of shRNA-p38 interfering plasmid in BMSCs. The protein expressions of p/t-p38, SOX9, collagen II, Aggrecan, p/t-Smad1, and p/t-Smad4, as well as the kinase activities of p38/ERK/JNK pathway, were investigated using Western blot analysis. Additionally, the level of chondroitin sulfate and glycosaminoglycans (GAG) expression were measured by Alcian blue staining and GAG assay kit via qualitative and quantitative methods, respectively.

resultsThe results demonstrated that p38 pathway was activated in the chondrogenic differentiation of BMSCs induced by TGF-β1. Cartilage-specific genes and chondrogenic regulators, such as SOX9, collagen II, Aggrecan, and GAG, were upregulated by TGF-β1, which could be reversed by predisposed with shRNA-p38 interfering plasmid and p38-MAPK inhibitors (SB203580). Moreover, the activation of p38/ERK/JNK pathways in the presence of TGF-β1 was suppressed by shRNA-p38 and SB203580 treatment.

conclusionCollectively, the activation of p38/ERK/JNK/Smad pathways plays a facilitated role in the chondrogenic differentiation induced by TGF-β1. After suppressing the p38 pathway, the chondrogenesis can be inhibited, which can be used to guide the treatment of osteoarthritis.

Indexed as

Cell DifferentiationCells, CulturedChondrogenesisDown-RegulationEnzyme ActivationGene Expression RegulationHumansMAP Kinase Signaling SystemMesenchymal Stem Cellsp38 Mitogen-Activated Protein KinasesTransforming Growth Factor beta1p38 Mitogen-Activated Protein KinasesTransforming Growth Factor beta1BMSCsChondrogenic differentiationOsteoarthritisp38-MAPKTGF-β1

Identifiers

PMID31831024
PMCPMC6909593
OpenAlexW2996659356

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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.