AI Article Synopsis
- RANKL is a key regulator that enhances the movement of monocytes by activating specific signaling pathways involving phosphatidylinositol 3-kinase, phosphodiesterase, and Src kinases.
- The study used various methods, like micropore filter assays and Western blot analysis, to observe how RANKL influences monocyte locomotion and to confirm the presence of the RANK receptor in these cells.
- The findings indicate that RANK-expressing monocytes, when activated by RANKL, undergo directed migration, which can be inhibited by osteoprotegerin, a decoy receptor for RANKL.
Article Abstract
Objective: RANKL, a member of the tumor necrosis factor superfamily, is a central regulator of osteoclast recruitment and activation. Whether RANKL affects monocyte locomotion in vitro via RANK and a possible signaling pathway were investigated.
Methods: Monocytes were obtained from venous blood of healthy donors. Cell migration was studied by micropore filter assays. The signaling mechanisms required for RANKL-dependent migration were tested using signaling enzyme blockers and Western blot analyses. Expression of RANK messenger RNA (mRNA) in monocytes was demonstrated by reverse transcriptase-polymerase chain reaction, and receptor expression on cell surface was investigated by fluorescence-activated cell sorting analyses.
Results: RANKL significantly stimulated monocyte chemotaxis via activation of phosphatidylinositol 3-kinase, phosphodiesterase, and Src kinase. The effect on migration was inhibited by osteoprotegerin, which is the decoy receptor for RANKL. Expression of RANK receptor mRNA was shown, and synthesis of RANK in monocytes was suggested by the detection of RANK immunoreactivity on the cell surface.
Conclusion: These data suggest that RANK is expressed by monocytes whose activation by RANKL stimulates directed migration involving phosphatidylinositol 3-kinase, phosphodiesterase, and Src kinases.
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| http://dx.doi.org/10.1002/art.20352 | DOI Listing |
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