Targeting vascular endothelial growth factor ameliorates PMMA-particles induced inflammatory osteolysis in murine calvaria.


Journal

Bone
ISSN: 1873-2763
Titre abrégé: Bone
Pays: United States
ID NLM: 8504048

Informations de publication

Date de publication:
06 2019
Historique:
received: 08 01 2019
revised: 07 03 2019
accepted: 19 03 2019
pubmed: 25 3 2019
medline: 7 7 2020
entrez: 25 3 2019
Statut: ppublish

Résumé

Cytokines and growth factors mediate inflammatory osteolysis in response to particles released from bone implants. However, the mechanism by which this process develops is not entirely clear. Blood vessels and related factors may be required to deliver immune cells and soluble factors to the injury site. Therefore, in the current study we investigated if, vascular endothelial growth factor (VEGF), which is required for angiogenesis, mediates polymethylmethacrylate (PMMA) particles-induced osteolysis. Using bone marrow derived macrophages (BMMs) and ST2 stromal cell line, we show that PMMA particles increase VEGF expression. Further, using a murine calvarial osteolysis model, we found that PMMA injection over calvaria induce significant increase in VEGF expression as well as new vessel formation, represented by von Willebrand factor (vWF) staining. Co-treatment using a VEGF-neutralizing antibody abrogated expression of vWF, indicating decreased angiogenesis. Finally, VEGF neutralizing antibody reduced expression of Tumor necrosis factor (TNF) and decreased osteoclastogenesis induced by PMMA particles in calvariae. This work highlights the significance of angiogenesis, specifically VEGF, as key driver of PMMA particle-induced inflammatory osteolysis, inhibition of which attenuates this response.

Identifiants

pubmed: 30904629
pii: S8756-3282(19)30109-7
doi: 10.1016/j.bone.2019.03.025
pmc: PMC6491226
mid: NIHMS1525642
pii:
doi:

Substances chimiques

Bone Cements 0
Vascular Endothelial Growth Factor A 0
vascular endothelial growth factor A, mouse 0
Polymethyl Methacrylate 9011-14-7

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

86-91

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR072623
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR049192
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007200
Pays : United States
Organisme : NIAMS NIH HHS
ID : P30 AR057235
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR054326
Pays : United States

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

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Auteurs

Wahid Abu-Amer (W)

Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, United States of America.

Manoj Arra (M)

Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, United States of America.

John C F Clohisy (JCF)

Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, United States of America.

Yousef Abu-Amer (Y)

Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, United States of America; Department of Cell Biology & Physiology, Washington University School of Medicine, St. Louis, MO 63110, United States of America; Shriners Hospital for Children, St. Louis, MO 63110, United States of America.

Gaurav Swarnkar (G)

Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO 63110, United States of America. Electronic address: gauravswarnkar@wustl.edu.

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Classifications MeSH