Lee, S.H., Rho, J., Jeong, D., Sul, J.Y., Kim, T., Kim, N., Kang, J.S., Miyamoto, T., Suda, T., Lee, S.K., Pignolo, R.J., Koczon-Jaremko, B., Lorenzo, J. and Choi, Y. (2006) v-ATPase V0 Subunit d2-Deficient Mice Exhibit Impaired Osteoclast Fusion and Increased Bone Formation. Nature Medicine, 12, 1403-1409.
http://dx.doi.org/10.1038/nm1514

has been cited by the following article:

• TITLE: Joint Damage Accelerating Properties of Neutrophils

  AUTHORS: Viktoriya Milanova, Nina Ivanovska, Petya Dimitrova

  KEYWORDS: Neutrophils, RANKL, Cell Transfer, Zymosan, Osteoclasts

  JOURNAL NAME: Open Journal of Rheumatology and Autoimmune Diseases, Vol.4 No.2, May 22, 2014

  ABSTRACT: Neutrophils are innate immune cells involved in the initial inflammatory response and in the pathogenesis of rheumatoid arthritis (RA), an inflammatory joint disease. They produce cytokines, chemokines, proinflammatory mediators and secrete enzymes causing a direct destruction of cartilage and bone. Herein we investigated the ability of neutrophils to express the receptor activator of nuclear factor kappa-B ligand (RANKL) and to interfere with maturation of late pre-osteoclasts. The distribution of bone marrow (BM) Ly6G+ cells expressing RANKL was evaluated after BM cell dye labelling and transfer into zymosan-injected SCID recipient mice. Specific tartrate-resistant acid phosphatase (TRAP) staining was used to determine the number of multinucleated mature osteoclasts in the co-cultures of purified blood neutrophils with preosteoclasts. Ly6 G+ BM cells migrated extensively in synovial fluid and spleen of recipient zymosan-injected SCID mice. Labelled neutrophils have higher RANKL expression in synovial fluid unlike in spleen indicating that they obtained specific phenotype during their migration to the synovial fluid. Blood neutrophils increased the number of multinucleated mature osteoclasts in vitro. This effect was elicited by the pretreatment of neutrophils with interleukin (IL)-17. In summary, our study showed neutrophils’s properties to accelerate joint damage via RANKL and interactions with osteoclasts.