NDLI: Vinculin regulates osteoclast function.

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Vinculin regulates osteoclast function.

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Vinculin regulates osteoclast function.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Warren, Julia T. Teitelbaum, Steven L. Fukunaga, Tomohiro Zou, Wei
Description	Author Affiliation: Fukunaga T ( From the Departments of Pathology and Immunology and.)
Abstract	Osteoclastic bone resorption depends upon the cell's ability to organize its cytoskeleton. Because vinculin (VCL) is an actin-binding protein, we asked whether it participates in skeletal degradation. Thus, we mated VCL(fl/fl) mice with those expressing cathepsin K-Cre (CtsK-VCL) to delete the gene in mature osteoclasts or lysozyme M-Cre (LysM-VCL) to target all osteoclast lineage cells. VCL-deficient osteoclasts differentiate normally but, reflecting cytoskeletal disorganization, form small actin rings and fail to effectively resorb bone. In keeping with inhibited resorptive function, CtsK-VCL and LysM-VCL mice exhibit a doubling of bone mass. Despite cytoskeletal disorganization, the capacity of VCL(-/-) osteoclastic cells to normally phosphorylate c-Src in response to vß3 integrin ligand is intact. Thus, integrin-activated signals are unrelated to the means by which VCL organizes the osteoclast cytoskeleton. WT VCL completely rescues actin ring formation and bone resorption, as does VCL(P878A), which is incapable of interacting with Arp2/3. As expected, deletion of the VCL tail domain (VCL(1-880)), which binds actin, does not normalize VCL(-/-) osteoclasts. The same is true regarding VCL(I997A), which also prevents VCL/actin binding, and VCL(A50I) and VCL(811-1066), both of which arrest talin association. Thus, VCL binding talin, but not Arp2/3, is critical for osteoclast function, and its selective inhibition retards physiological bone loss.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	19
Volume Number	289
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2014-05-09
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Bone Resorption Metabolism Cytoskeleton Osteoclasts Vinculin Actin-Related Protein 2-3 Complex Genetics Actins Amino Acid Substitution Animals Pathology Mice Mice, Transgenic Mutation, Missense Protein Binding Protein Structure, Tertiary Talin Src-Family Kinases Research Support, N.I.H., Extramural Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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