파골세포 분화능을 세포사로 억제하는 알렌드로네이트의 효과
분야
의약학 > 의공학
저자
윤영필 ( Young Pil Yun ) , 김성은 ( Sung Eun Kim ) , 문호진 ( Ho Jin Moon ) , 권일근 ( Il Keun Kwon )
발행기관
한국조직공학·재생의학회
간행물정보
조직공학과 재생의학 2009년, 제6권 제4호, 603~608페이지(총6페이지)
파일형식
2a800379.pdf [무료 PDF 뷰어 다운로드]
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    영문초록
    Osteoclasts regulate bone homeostasis and have a key role in bone degenerative processes. Mouse RAW264.7 macrophage cells have been shown to retain the capacity to differentiate into osteoclast-like cells in the presence of a receptor activator of nuclear factor kappa B ligand(RANKL), which is essential and sufficient to promote the maturation of osteoclasts. When treated with RANKL, RAW264.7 cells express high levels of osteoclastassociated genes such as tartrate-resistant acid phosphatase(TRAP), which has been widely used to assess bone resorption. In this study, we hypothesized that alendronate prevents RANKL-induced osteoclast-like cells, which are known to play important roles in the bone-resorptive responses. We investigated that occurred TRAP-positive area and the expression patterns of two important proteolytic enzymes, cathepsin K and Matrix Metalloproteinase- 9(MMP-9) during RANKL-induced osteoclast differentiation in RAW264.7 cells. These results showed that increased TRAP-positive staining and both cathepsin K and MMP-9 mRNA expression levels on RANKL-induced osteoclast differentiation during 4 days. Especially, alendronate increased caspase-3 expression for apoptosis with Western blot analysis. These results showed that alendronate cause apoptosis and thus osteoclast differentiation inhibit. This finding may help the understanding of the osteolytic and osteoporotic processes responsible for bone diseases, including osteoporosis and periodontal diseases.
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