The effects of P2X7 receptor antagonists on the formation and function of human osteoclasts in vitro

The P2X7 receptor (P2X7R) has been implicated in the process of multinucleation and cell fusion. We have previously demonstrated that blockade of P2X7Rs on osteoclast precursors using a blocking antibody inhibited multinucleated osteoclast formation in vitro, but that P2X7R KO mice maintain the abil...

Full description

Saved in:
Bibliographic Details
Published inPurinergic signalling Vol. 6; no. 3; pp. 307 - 315
Main Authors Agrawal, Ankita, Buckley, Katherine A., Bowers, Keith, Furber, Mark, Gallagher, James A., Gartland, Alison
Format Journal Article
LanguageEnglish
Published Dordrecht Springer Netherlands 01.09.2010
Subjects
Biomedical and Life Sciences
Biomedicine
Cancer Research
Human Physiology
Neurosciences
Original
Original Article
Pharmacology/Toxicology
P2X7
P2 receptor
Resorption
Osteoclast
ATP
Formation
Fusion
Online AccessGet full text

Cover

More Information
Summary:The P2X7 receptor (P2X7R) has been implicated in the process of multinucleation and cell fusion. We have previously demonstrated that blockade of P2X7Rs on osteoclast precursors using a blocking antibody inhibited multinucleated osteoclast formation in vitro, but that P2X7R KO mice maintain the ability to form multinucleated osteoclasts. This apparent contradiction of the role the P2X7R plays in multinucleation has prompted us to examine the effect of the most commonly used and recently available P2X7R antagonists on osteoclast formation and function. When added to recombinant RANKL and M-CSF human blood monocytes cultures, all but one compound, decreased the formation and function of multinucleated TRAP-positive osteoclasts in a concentration-dependent manner. These data provide further evidence for the role of the P2X7R in the formation of functional human multinucleated osteoclasts and highlight the importance of selection of antagonists for use in long-term experiments.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Article-2
ObjectType-Feature-1
ISSN:1573-9538
1573-9546
DOI:10.1007/s11302-010-9181-z