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Submitted on September 24, 2004
Accepted on February 15, 2005
Division of General Internal Medicine, Department of Internal Medicine, Medical University of Innsbruck, Innsbruck, Austria
* To whom correspondence should be addressed. E-mail: christian.wiedermann{at}uibk.ac.at.
Chronic inflammation is characterized by tissue infiltration with monocytes/macrophages which possess broad proinflammatory, destructive and remodeling capacities. Elevated levels of Osteoprotegerin, an important regulator of differentiation and activation of osteoclasts that also affects different cells of the immune system, were found in the serum of patients with chronic inflammatory diseases. The study of whether osteoprotegerin affects monocyte locomotion in vitro and the possible mechanisms and pathways involved was investigated using Boyden microchemotaxis chambers and Western blot analyses. Osteoprotegerin significantly stimulated monocyte chemotaxis, while pre-incubation of monocytes with osteoprotegerin inhibited monocyte migration toward optimal concentrations of RANTES, monocyte chemotactic protein-1 and procalcitonin. The effects of osteoprotegerin were abolished by pre-treating cells with heparinase I and chondroitinase or antibodies against the ectodomain of syndecan-1. Osteoprotegerin signaling was shown to involve protein kinase C, phosphatidylinositol 3-kinase/ Akt and tyrosine kinase.
Data suggest that osteoprotegerin affects monocyte migration and protein kinase C and phosphatidylinositol 3-kinase/ Akt activation via syndecan-1. Osteoprotegerin-induced deactivation of monocyte chemotaxis toward different chemokines is due to interaction of osteoprotegerin with heparan sulfate and chondroitin sulfate.
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