Evidence map›Paper›PMID 32436939›Full record

ArticleBioscience reports2020

Pentraxin 3 promotes the osteoblastic differentiation of MC3T3-E1 cells through the PI3K/Akt signaling pathway.

Yong Liu, Hui Wang, Xiao-Zhe Zhou, Ning Li, Yi-Chao Guo, Tao-Ping Chen

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Osteogenic Effects ofFoods (Basel, Switzerland) · 2026
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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

6 authors at 5 institutions in 1 country.

Yong LiuDepartment of Orthopedics, The People's Hospital of Suzhou New District, Suzhou, Jiangsu 215129, China.
Hui WangDepartment of Orthopedics, The General Hospital of JiZhong Energy Fengfeng Group Co., LTD., 28 North Fuhe Street, Handan 056002, China.
Xiao-Zhe ZhouDepartment of Orthopedics, Affiliated Hospital of Hebei University, Baoding 071000, China.
Ning LiDepartment of Minimally Invasive Spine Surgery, Tianjin Hospital, Tianjin, China.
Yi-Chao GuoDepartment of Orthopedics, Baoding Orthopaedic Hospital/People's Hospital of Lianchi District, Baoding, China.
Tao-Ping ChenDepartment of Orthopedics, Affiliated Hospital of Hebei University, Baoding 071000, China.
Affiliated Hospital of Hebei University · CNBaoding People's Hospital · CNDongfeng General Hospital · CNThe Fifth People’s Hospital of Suzhou · CNTianjin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoblast cells are responsible for synthesizing new bone tissue, and determining how to control osteoblastic differentiation is vital to the treatment of osteoporosis. In the present study, we show that pentraxin 3 (PTX3) signaling is involved in the regulation of osteoblastic differentiation in MC3T3-E1 cells. Our data reveal that PTX3 is abundantly expressed in MC3T3-E1 cells and that its expression is inducible by the introduction of osteogenic induction medium (OIM). Overexpression of PTX3 was observed to significantly increase the expression of four osteoblast signature genes, including Runt-related transcription factor 2 (RUNX2), alkaline phosphatase (ALP), osteocalcin (OCN) and osterix (OSX), suggesting that the overexpression of PTX3 promotes osteoblastic differentiation. The relative level of gene expression between OIM and OIM plus overexpressed PTX3 was evaluated using the Affymetrix Gene Chip® mouse gene microarray. PTX3-related differentially expressed genes (DEGs) were screened. Gene ontology (GO) functional and Kyoto Encyclopedia of Genes and Genomes database (KEGG) pathway enrichment analyses were performed, and the PI3K/Akt signaling pathway was primarily involved in the osteogenic differentiation of PTX3. Protein-protein interactions (PPIs) were also constructed, and the molecular complex detection (MCODE) plugin calculated modules of PPI networks. Moreover, we show that the effect of PTX3 is mediated by its induction of the PI3K/Akt signaling pathway. Mechanistically, we show that the action of PTX3 requires the activation of PI3K and Akt, and deactivation of PI3K by its inhibitor LY294002 weakens the PTX3-mediated induction of osteoblast signature genes, ALP and matrix mineralization. The present study revealed a new role played by PTX3 and suggest a potential mechanism governing the osteoblastic differentiation of MC3T3-E1 cells.

Indexed as

Cell DifferentiationOsteogenesis3T3 CellsAlkaline PhosphataseAnimalsCore Binding Factor Alpha 1 SubunitC-Reactive ProteinDatabases, GeneticGene Regulatory NetworksMiceNerve Tissue ProteinsOsteoblastsOsteocalcinPentraxinsPhosphatidylinositol 3-KinaseProtein Interaction MapsAlkaline PhosphataseCore Binding Factor Alpha 1 SubunitC-Reactive ProteinNerve Tissue ProteinsOsteocalcinPentraxinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRunx2 protein, mouseSp7 protein, mouseSp7 Transcription FactorMC3T3-E1 cellsOsteogenic differentiationPI3K/AktPTX3

Identifiers

PMID32436939
PMCPMC7284320
OpenAlexW3028374389

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.