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Involvement of receptor activator of nuclear factor kappaB ligand/osteoclast differentiation factor in osteoclastogenesis from synoviocytes in rheumatoid arthritis.
RANKL/ODF expressed on synovial fibroblasts is involved in rheumatoid bone destruction by inducing osteoclastogenesis and would therefore be a good therapeutic target.
Regulation by PGE2 of the production of interleukin‐6, macrophage colony stimulating factor, and vascular endothelial growth factor in human synovial fibroblasts
The results suggest that endogenous PGE2 regulates the production of IL‐6, M‐CSF, and VEGF by IL‐1β‐stimulated human synovial fibroblasts through the activation of EP2 and EP4 receptors with increase in cyclic AMP.
Vitamin K2 Enhances Osteocalcin Accumulation in the Extracellular Matrix of Human Osteoblasts In Vitro
  • Y. Koshihara, K. Hoshi
  • Biology, Materials Science
    Journal of bone and mineral research : the…
  • 1 March 1997
It is demonstrated that vitamin K2 enhanced not only the accumulation of Gla osteocalcin, but also the osteoccin production induced by 1,25(OH)2D3 in human osteoblasts in culture.
Mechanism of mustard oil-induced skin inflammation in mice.
Vitamin K stimulates osteoblastogenesis and inhibits osteoclastogenesis in human bone marrow cell culture.
Vitamin K might stimulate osteoblastogenesis in bone marrow cells, regulating osteoclastogenesis through the expression of RANKL/ODF more than through that of OPG/OCIF.
A new mechanism of bone destruction in rheumatoid arthritis: synovial fibroblasts induce osteoclastogenesis.
It is shown that osteoclast-like cells are formed in co-culture of peripheral blood mononuclear cells and rheumatoidsynovial fibroblasts obtained by continued sub-cultures, implicating that osteoclasts generated within the synovial membrane are probably involved in bone destruction in rhearatoid arthritis.
Suppression of arthritic bone destruction by adenovirus-mediated csk gene transfer to synoviocytes and osteoclasts.
Adenovirus-mediated direct transfer of the csk gene is useful in repressing bone destruction and inflammatory reactions, suggesting the involvement of Src family tyrosine kinases in arthritic joint breakdown and demonstrating the feasibility of intervention in the kinases for gene therapy in RA.
Profile of capsaicin‐induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid‐induced ear oedema
The results suggest that the mechanism of capsaicin‐induced ear oedema is different from that of AA‐induced oedma and suggest thatThe development of capsicin‐ induced ear oingema is primarily mediated by neuropeptides.