Inhibition of osteoclastogenesis by thioredoxin-interacting protein-derived peptide (TN13)

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Inhibition of osteoclastogenesis by thioredoxin-interacting protein-derived peptide (TN13)
Mi Jeong Kim; Won Sam Kim; Jae-Eun Byun; Jung Ha Choi; Suk Ran Yoon; In Pyo Choi; Haiyoung Jung
Bibliographic Citation
Journal of Clinical Medicine, vol. 8, no. 4, pp. 431-431
Publication Year
Overactivated osteoclasts lead to many bone diseases, including osteoporosis and rheumatoid arthritis. The p38 MAPK (p38) is an essential regulator of the receptor activator of nuclear factor- B ligand (RANKL)-mediated osteoclastogenesis and bone loss. We previously reported TAT conjugated thioredoxin-interacting protein-derived peptide (TAT-TN13) as an inhibitor of p38 in hematopoietic stem cells (HSCs). Here, we examined the role of TAT-TN13 in the differentiation and function of osteoclasts. TAT-TN13 significantly suppressed RANKL-mediated differentiation of RAW 264.7 cells and bone marrow macrophages (BMMs) into osteoclasts. TAT-TN13 also inhibited the RANKL-induced activation of NF- B and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), leading to the decreased expression of osteoclast-specific genes, including tartrate-resistant acid phosphatase (TRAP) and Cathepsin K. Additionally, TAT-TN13 treatment protected bone loss in ovariectomized (OVX) mice. Taken together, these results suggest that TAT-TN13 inhibits osteoclast differentiation by regulating the p38 and NF- B signaling pathway; thus, it may be a useful agent for preventing or treating osteoporosis.
osteoporosisosteoclastosteoclastogenesisp38 MAPKTAT-TN13ovariectomy
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Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Aging Convergence Research Center > 1. Journal Articles
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