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Cyclic tensile stress inhibits Wnt/β-catenin signaling in human periodontal ligament cells
Kim, Ji Young,Yang, Daum,Kim, Ha-Neui,Jung, Kyoung Suk,Chang, Young Il,Lee, Zang Hee KOREAN ACADAMY OF ORAL BIOLOGY 2009 International Journal of Oral Biology Vol.34 No.2
Periodontal ligament (PDL) tissue is a connective tissue that is interposed between the roots of the teeth and the inner wall of the alveolar bone socket. PDL is always exposed to physiologic mechanical force such as masticatoryforce and PDL cells play important roles during orthodontic tooth movement by synthesizing and secreting different mediators involved in bone remodeling. The Wntβ-catenin signaling pathway was recently shown to play a significant role in the control of bone formation. In the present study, we applied cyclic tensile stress of 20% elongation to cultured human PDL cells and assessed its impact after six days upon components of the Wnt/β-catenin signaling pathway. RT-PCR analysis showed that Wnt1a, Wnt3a, Wnt10b and the Wnt receptor LRP5 were down-regulated, whereas the Wnt inhibitor DKK1 was up-regulated in response to these stress conditions. In contrast, little change was detected in the mRNA expression of Wnt5a, Wnt7b, Fz1, and LRP6. By western blotting we found decreased expression of the β-catenin and p-GSK-3(3β proteins. Our results thus show that mechanical stress suppresses the canonical Wnt/β-catenin signaling pathway in PDL cells.
Poster Session : ERK and Akt prevent osteoclasts apoptosis through blockage caspase-9 and -3
( Han Bok Kwak ),( Daum Yang ),( Hyun Min Sun ),( Hyun Il Ha ),( Ha Neui Kim ),( Jong Ho Lee ),( Kyoung Suk Jeong ),( Hong Hee Kim ),( Zang Hee Lee ) 한국생화학분자생물학회 (구 한국생화학회) 2006 생화학분자생물학회 춘계학술발표논문집 Vol.2006 No.-
Trolox Prevents Osteoclastogenesis by Suppressing RANKL Expression and Signaling
Lee, Jong-Ho,Kim, Ha-Neui,Yang, Daum,Jung, Kyoungsuk,Kim, Hyun-Man,Kim, Hong-Hee,Ha, Hyunil,Lee, Zang Hee American Society for Biochemistry and Molecular Bi 2009 The Journal of biological chemistry Vol.284 No.20
<P>Excessive receptor activator of NF-kappaB ligand (RANKL) signaling causes enhanced osteoclast formation and bone resorption. Thus, down-regulation of RANKL expression or its downstream signals may be a therapeutic approach to the treatment of pathological bone loss. In this study, we investigated the effects of Trolox, a water-soluble vitamin E analogue, on osteoclastogenesis and RANKL signaling. Trolox potently inhibited interleukin-1-induced osteoclast formation in bone marrow cell-osteoblast coculture by abrogating RANKL induction in osteoblasts. This RANKL reduction was attributed to the reduced production of prostaglandin E(2) via a down-regulation of cyclooxygenase-2 activity. We also found that Trolox inhibited osteoclast formation from bone marrow macrophages induced by macrophage colony-stimulating factor plus RANKL in a reversible manner. Trolox was effective only when present during the early stage of culture, which implies that it targets early osteoclast precursors. Pretreatment with Trolox did not affect RANKL-induced early signaling pathways, including MAPKs, NF-kappaB, and Akt. We found that Trolox down-regulated the induction by RANKL of c-Fos protein by suppressing its translation. Ectopic overexpression of c-Fos rescued the inhibition of osteoclastogenesis by Trolox in bone marrow macrophages. Trolox also suppressed interleukin-1-induced osteoclast formation and bone loss in mouse calvarial bone. Taken together, our findings indicate that Trolox prevents osteoclast formation and bone loss by inhibiting both RANKL induction in osteoblasts and c-Fos expression in osteoclast precursors.</P>