Evidence map›Paper›PMID 37565509›Full record

ArticleAnimal models and experimental medicine2023

Platelet factor 4 induces bone loss by inhibiting the integrin α5-FAK-ERK pathway.

Wei Li, Qiwei Zhang, Ranli Gu, Lijun Zeng, Hao Liu

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

Article in Animal models and experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Role and mechanism of Integrin α5β1 in bone formation and disease.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. 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

5 authors at 2 institutions in 2 countries.

Wei LiDepartment of Oral Pathology, Peking University School and Hospital of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing Key Laboratory of Digital Stomatology, National Health Commission Key Laboratory of Digital Technology of Stomatology, Peking University, Beijing, China.
Qiwei ZhangDepartment of Orthopedics, Beijing Hospital and National Center of Gerontology and Institute of Geriatrics Medicine, Chinese Academy of Medical Sciences, Beijing, China.
Ranli GuDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing Key Laboratory of Digital Stomatology, National Health Commission Key Laboratory of Digital Technology of Stomatology, Peking University, Beijing, China.
Lijun ZengDepartment of Prosthodontics, Peking University School and Hospital of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing Key Laboratory of Digital Stomatology, National Health Commission Key Laboratory of Digital Technology of Stomatology, Peking University, Beijing, China.
Hao LiuThe Central Laboratory, Peking University School and Hospital of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing Key Laboratory of Digital Stomatology, National Health Commission Key Laboratory of Digital Technology of Stomatology, Peking University, Beijing, China.ORCID 0000-0003-0977-5884
Peking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

Beijing Natural Science Foundation L222145CAMS Innovation Fund for Medical Sciences 2019-I2M-5-038Clinical Medicine Plus X - Young Scholars Project, Peking University, the Fundamental Research Funds for the Central Universities PKU2023LCXQ017National Natural Science Foundation of China 81700935
6 · The paper itself

Abstract

backgroundThe effect of platelet factor 4 (PF4) on bone marrow mesenchymal stem cells (BMMSCs) and osteoporosis is poorly understood. Therefore, this study aimed to evaluate the effects of PF4-triggered bone destruction in mice and determine the underlying mechanism.

methodsFirst, in vitro cell proliferation and cell cycle of BMMSCs were assessed using a CCK8 assay and flow cytometry, respectively. Osteogenic differentiation was confirmed using staining and quantification of alkaline phosphatase and Alizarin Red S. Next, an osteoporotic mouse model was established by performing bilateral ovariectomy (OVX). Furthermore, the PF4 concentrations were obtained using enzyme-linked immunosorbent assay. The bone microarchitecture of the femur was evaluated using microCT and histological analyses. Finally, the key regulators of osteogenesis and pathways were investigated using quantitative real-time polymerase chain reaction and Western blotting.

resultsHuman PF4 widely and moderately decreased the cell proliferation and osteogenic differentiation ability of BMMSCs. Furthermore, the levels of PF4 in the serum and bone marrow were generally increased, whereas bone microarchitecture deteriorated due to OVX. Moreover, in vivo mouse PF4 supplementation triggered bone deterioration of the femur. In addition, several key regulators of osteogenesis were downregulated, and the integrin α5-focal adhesion kinase-extracellular signal-regulated kinase (ITGA5-FAK-ERK) pathway was inhibited due to PF4 supplementation.

conclusionsPF4 may be attributed to OVX-induced bone loss triggered by the suppression of bone formation in vivo and alleviate BMMSC osteogenic differentiation by inhibiting the ITGA5-FAK-ERK pathway.

Indexed as

Integrin alpha5OsteogenesisAnimalsCells, CulturedExtracellular Signal-Regulated MAP KinasesFemaleFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesHumansMAP Kinase Signaling SystemMiceMitogen-Activated Protein Kinase KinasesPlatelet Factor 4Extracellular Signal-Regulated MAP KinasesFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesIntegrin alpha5Mitogen-Activated Protein Kinase KinasesPlatelet Factor 4PTK2 protein, humanbone lossbone marrow mesenchymal stem cellsintegrin α5osteogenesisplatelet factor 4

Identifiers

PMID37565509
PMCPMC10757219
OpenAlexW4385752002

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.