Evidence map›Paper›PMID 33833129›Full record

ArticleAging2021

COX-2 promotes the osteogenic potential of BMP9 through TGF-β1/p38 signaling in mesenchymal stem cells.

Yan Deng, Ling Li, Jia-Hui Zhu, Pei-Pei Li, Yi-Xuan Deng, Hong-Hong Luo, Yuan-Yuan Yang, Bai-Cheng He, Yuxi Su

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Lactic Acid Bacteria Metabolites Modulate Immune Response AgainstAnimals : an open access journal from MDPI · 2025
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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

9 authors at 3 institutions in 1 country.

Yan DengDepartment of Orthopedics, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Ling LiKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Jia-Hui ZhuKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Pei-Pei LiKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Yi-Xuan DengKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Hong-Hong LuoKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Yuan-Yuan YangKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Bai-Cheng HeKey Laboratory of Biochemistry and Molecular Pharmacology of Chongqing, Chongqing Medical University, Chongqing 400016, China.
Yuxi SuDepartment of Orthopedics, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Chongqing Medical University · CNChildren's Hospital of Chongqing Medical University · CNChina International Science and Technology Cooperation · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study investigated the effects of transforming growth factor-β1 (TGF-β1) and cyclooxygenase-2 (COX-2) on bone morphogenetic protein 9 (BMP9) in mesenchymal stem cells (MSCs). We found that BMP9 increased mRNA levels of TGF-β1 and COX-2 in C3H10T1/2 cells. BMP9-induced osteogenic markers were enhanced by TGF-β1 and reduced by TGF-βRI-specific inhibitor LY364947. BMP9 increased level of p-Smad2/3, which were either enhanced or reduced by COX-2 and its inhibitor NS398. BMP9-induced osteogenic markers were decreased by NS398 and it was partially reversed by TGF-β1. COX-2 increased BMP9-induced osteogenic marker levels, which almost abolished by LY364947. BMP9-induced bone formation was enhanced by TGF-β1 but reduced by silencing TGF-β1 or COX-2. BMP9's osteogenic ability was inhibited by silencing COX-2 but partially reversed by TGF-β1. TGF-β1 and COX-2 enhanced activation of p38 signaling, which was induced by BMP9 and reduced by LY364947. The ability of TGF-β1 to increase the BMP9-induced osteogenic markers was reduced by p38-specific inhibitor, while BMP9-induced TGF-β1 expression was reduced by NS398, but enhanced by COX-2. Furthermore, CREB interacted with Smad1/5/8 to regulate TGF-β1 expression in MSCs. These findings suggest that COX-2 overexpression leads to increase BMP9's osteogenic ability, resulting from TGF-β1 upregulation which then activates p38 signaling in MSCs.

Indexed as

AnimalsCell LineCyclooxygenase 2FemaleGene Knockdown TechniquesGrowth Differentiation Factor 2MAP Kinase Signaling SystemMesenchymal Stem CellsMiceModels, AnimalOsteogenesisp38 Mitogen-Activated Protein KinasesReceptor, Transforming Growth Factor-beta Type ITransforming Growth Factor beta1Cyclooxygenase 2Gdf2 protein, mouseGrowth Differentiation Factor 2p38 Mitogen-Activated Protein KinasesPtgs2 protein, mouseReceptor, Transforming Growth Factor-beta Type ITgfb1 protein, mouseTgfbr1 protein, mouseTransforming Growth Factor beta1BMP9COX-2osteogenic differentiationp38 MAPKTGF-β1

Identifiers

PMID33833129
PMCPMC8109063
OpenAlexW3150865151

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.