Assistant Professor, Department of Medicine, Weill Medical College of Cornell University
Assistant Scientist, Arthritis and Tissue Degeneration Program, Hospital for Special Surgery
Zhao B, Katagiri T, Toyoda H, Takada T, Yanai T, Fukuda T, Chung U, Koike T, Takaoka K, and Kamijo R. Heparin Potentiates the in Vivo Ectopic Bone Formation Induced by Bone Morphogenetic Protein-2. Journal of Biological Chemistry, 281(32), 23246-23253, 2006. PMID: 16754660
Mochizuki A, Takami M, Kawawa T, Suzumoto R, Sasaki T, Shiba A, Tsukasaki H, Zhao B, Yasuhara R, Suzawa T, Miyamoto Y, Choi Y, and Kamijo R. Identification and characterization of the precursors committed to osteoclasts induced by TNF-related activation-induced cytokine/receptor activator of NF-kappa B ligand. Journal of Immunology, 177: 4360 – 4368, 2006. PMID: 16982870
Yamada A, Takami M, Kawawa T, Yasuhara R, Zhao B, Mochizuki A, Miyamoto Y, Eto T, Yasuda H, Nakamichi Y, Kim N, Katagiri T, Suda T, Kamijo R. Interleukin-4 inhibition of osteoclast differentiation is stronger than that of interleukin-13 and they are equivalent for induction of osteoprotegerin production from osteoblasts Immunology 120 (4), 573–579, 2007. PMC2265899
Zhao B, Takami M, Miyamoto Y, Suzawa T, Yamada A, Mochizuki A, Yasuhara R, Wang X, Inoue T, Namiki O, Sakamoto K, Kamijo R. Characterization of synovial cell clones isolated from rheumatoid arthritis patients: possible involvement of TNF-alpha in reduction of osteoprotegerin in synovium. Cytokine, 41, 61-70, 2008. PMID: 18083042
Zhao B, Takami M, Kamijo R. Regulation of Osteoclast Differentiation by Toll-like receptors (TLRs). J Tissue Cult Dent Res. 17(2): p33-39, 2008.
Takami M, Mochizuki A, Yamada A, Tachi K, Zhao B, Miyamoto Y, Anada T, Honda Y, Inoue T, Nakamura M, Suzuki O, Kamijo R. Osteoclast differentiation induced by synthetic octacalcium phosphate through RANKL expression in osteoblasts. Tissue Eng Part A. 15: 3991-4000, 2009. PMID: 19594360
Zhao B, Takami M, Yamada A, Wang X, Koga T, Hu X, Tamura T, Ozato K, Choi Y, Ivashkiv LB, Takayanagi H, Kamijo R. Interferon regulatory factor 8 regulates bone metabolism by suppressing osteoclastogenesis. Nature Medicine 15:1066-1071, 2009. PMC2755267
Kalliolias G, Zhao B, Triantafyllopoulou A, Park-Min K, Ivashkiv L. IL-27 inhibits human osteoclastogenesis by abrogating RANKL-mediated induction of NFATc1 and suppressing proximal RANK signaling. Arthritis & Rheumatology, 62(2):402-13, 2010. PMC2822027
Zhao B, Ivashkiv L. Negative regulation of osteoclastogenesis and bone resorption by cytokines and transcriptional repressors. Arthritis Research & Therapy, 13(4): 234, 2011. PMC3239342
Ivashkiv L, Zhao B, Park-Min KH, Takami M. Feedback inhibition of osteoclastogenesis during inflammation by IL-10, M-CSF receptor shedding, and induction of IRF8. Ann N Y Acad Sci., 1237: 88-94, 2011. PMC3263822
Zhao B, Grimes S, Li S, Hu X, Ivashkiv L. TNF-induced Osteoclastogenesis and Inflammatory Bone Resorption are Inhibited by Transcription Factor RBP-J. Journal of Experimental Medicine, 209(2): 319-34, 2012. PMC3280875
Xu H, Zhu J, Smith S, Foldi J, Zhao B, Chung A, Outtz H, Kitajewski J, Shi C, Weber S, Saftig P, Li Y, Ozato K, Blobel C, Ivashkiv L, Hu X. Notch-RBP-J Signaling Regulates IRF8 to Promote Inflammatory Macrophage Polarization. Nature Immunology, 13(7): 642-50, 2012. PMC3513378
Zhao R, Wang A, Hall KC, Otero M, Weskamp G, Zhao B, Hill D, Goldring MB, Glomski K, Blobel CP. Lack of ADAM10 in endothelial cells affects osteoclasts at the chondro-osseus junction. J Orthop Res., 32:224–230, 2014. PMID: 24108673
Park-Min K, Lim E, Lee M, Park S, Giannopoulou E, Yarilina A, Meulen M, Zhao B, Smithers N, Witherington J, Lee K, Tak P, Prinjha R, Ivashkiv L. Inhibition of osteoclastogenesis and inflammatory bone resorption by targeting BET proteins and epigenetic regulation. Nature Communications, 2014 Nov 13;5:5418. doi: 10.1038/ncomms6418
Li S, Miller C, Giannopoulou E, Hu X, Ivashkiv L , Zhao B. RBP-J imposes a requirement for ITAM-mediated costimulation of osteoclastogenesis. Journal of Clinical Investigation, 2014 Nov 3;124(11):5057-73
For more publications, please see the PubMed listing.
Bone destruction is a severe consequence of many diseases associated with osteolysis, including rheumatoid arthritis (RA) and peri-prosthetic loosening, and a major cause of morbidity and disability in inflammatory arthritis patients. We are particularly interested in the key inflammatory cytokine TNF-mediated osteoclastogenesis and bone resorption. By comparing with the physiological osteoclastogenic inducer RANKL, we have aimed to distinguish and identify novel regulators, for example IRF-8 and RBP-J, that predominantly control pathological bone resorption, thereby providing specific therapeutic targets for clinic with minimal side effects on physiological bone remodeling. We employ a combination of molecular and cellular approaches as well as various mouse models, including the inflammatory arthritis model and osteoporosis model for our research. Besides the coding genes, we recently challenge a new field- genome wide study of non-coding RNAs (ncRNAs). By using modern genomic approaches including second-generation deep sequencing and bioinformatics analysis, we have successfully identified a few promising novel ncRNAs that were unable to reveal by traditional methods. We thus opened a pioneering research area studying non-coding genes in osteoclast biology and osteolysis.
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One of the goals of Hospital for Special Surgery (HSS) is to advance the science of orthopedic surgery, rheumatology, and related disciplines for the benefit of patients. Research staff at HSS may collaborate with outside companies for education, research and medical advances. HSS supports this collaboration in order to foster medical breakthroughs; however, HSS also believes that these collaborations must be disclosed.
As part of the disclosure process, this website lists Research staff collaborations with outside companies if the Research staff member received any payment during the prior year or expects to receive any payment in the next year. The disclosures are based on information provided by the Research staff and other sources and are updated regularly. Current ownership interests and leadership positions are also listed. Further information may be available on individual company websites.
As of April 21, 2015, Dr. Zhao reported no financial interest relationships with healthcare industry.
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