Bisphosphonate effects on capthesin K and bone resorption function during osteoclast differentiation / 中国组织工程研究
Chinese Journal of Tissue Engineering Research
;
(53): 5293-5298, 2014.
Artigo
em Chinês
| WPRIM
| ID: wpr-454416
ABSTRACT
BACKGROUND:
Studies have shown that bisphosphonates inhibit osteoclast resorption, but whether cathepsin K, a key cytokine of bone resorption, plays an effect has rarely been reported.OBJECTIVE:
To study the effect of bisphosphonate on capthesin K and bone resorption function during osteoclast differentiation.METHODS:
Osteoclasts were cultured by mouse monocyte-macrophage cellline-RAW264.7. The cells were divided into two groupscontrol group, treated with 100μg/L receptor activator of nuclear factorκB ligand factor;alendronate group, treated with 100μg/L receptor activator of nuclear factorκB ligand factor+10-7 mol/L alendronate. Osteoclastogenesis and resorption function of osteoclasts were examined at 7 days of culture and gene expression of capthesin K was detected by immunofluorescence method at 72 hours of culture. Western blot assay was used to detect capthesin K protein expression at 72 hours of culture. RESULTS ANDCONCLUSION:
Tartrate-resistant acid phosphatase positive multinuclear cells were observed and resorption lacunae formed in two groups. Control group showed the higher number of tartrate-resistant acid phosphatase positive multinuclear cells and larger size of resorption lacunae than the alendronate group (P<0.01). Immunofluorescence showed expression of capthesin K was higher in the control group than the alendronate group (P<0.01);furthermore, the protein expression of capthesin K was also lower in the alendronate group than the control group (P<0.01). These findings indicate that bisphosphonates could strongly inhibit osteoclastogenesis and its resorption function by inhibiting gene expression of capthesin K.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Journal of Tissue Engineering Research
Ano de publicação:
2014
Tipo de documento:
Artigo
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