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Cbfa1 induces the expression of the mineral-related proteins in human dental papilla cells / 中华口腔医学杂志
Chinese Journal of Stomatology ; (12): 271-274, 2003.
Artículo en Chino | WPRIM | ID: wpr-253725
ABSTRACT
<p><b>OBJECTIVE</b>To explicit whether the expression of the mineral-related proteins is regulated by cbfa1 in human dental papilla cells.</p><p><b>METHODS</b>Human dental papilla cells were cultured in vitro and transfected with pcDNA3-cbfa1 recombinant plasmids. After selected with G418 sulfate, a cell clone named PC-3, which could stably express the cbfa1 mRNA and protein, was proved by PCR and western blot. Then the amount of ALP and OC and the expression of OPN, BSP, ON, DMP1, DSP and DSPP were detected by immunohistochemistry, Western blot and PCR methods.</p><p><b>RESULTS</b>We established the human dental papilla cells model PC-3 which could stably express the cbfa1 mRNA and protein. Compared with normal cells, a lot of mineral-related proteins such as ALP, OC, OPN, BSP, ON, DMP1 were upregulated in PC-3 cells.</p><p><b>CONCLUSIONS</b>In human dental papilla cells, cbfa1 can induce the expression of most mineral-related genes and proteins. It may implicate that cbfa1 must play a key role during tooth development and mineralization.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Fisiología / Osteocalcina / Células Cultivadas / Biología Celular / Papila Dental / Fosfatasa Alcalina / Subunidad alfa 1 del Factor de Unión al Sitio Principal / Metabolismo Tipo de estudio: Estudio pronóstico Límite: Humanos Idioma: Chino Revista: Chinese Journal of Stomatology Año: 2003 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Fisiología / Osteocalcina / Células Cultivadas / Biología Celular / Papila Dental / Fosfatasa Alcalina / Subunidad alfa 1 del Factor de Unión al Sitio Principal / Metabolismo Tipo de estudio: Estudio pronóstico Límite: Humanos Idioma: Chino Revista: Chinese Journal of Stomatology Año: 2003 Tipo del documento: Artículo