4.3 Article

Influence of TGF-β1 on the expression of BSP, DSP, TGF-β1 receptor I and Smad proteins during reparative dentinogenesis

期刊

JOURNAL OF MOLECULAR HISTOLOGY
卷 39, 期 2, 页码 153-160

出版社

SPRINGER
DOI: 10.1007/s10735-007-9148-8

关键词

reparative dentin; transforming growth factor-beta 1; osteodentin; bone sialoprotein; dentin sialophosphoprotein

资金

  1. National Research Foundation of Korea [전06A1202, 전06A1204] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Reparative dentin has a wide variety of manifestations ranging from a regular, tubular form to an irregular, atubular form. However, the characteristics of reparative dentin have not been clarified. This study hypothesized that the level of bone sialoprotein (BSP) expression will increase if the newly formed reparative dentin is bone-like but the dentin sialophosphoprotein (DSPP) level will decrease. In order to test this hypothesis, the expression of BSP and DSP was examined by immunohistochemistry and the expression of BSP was measured by in situ hybridization in an animal model. The pulps of 12 maxillary right first molars from twelve male rats were exposed and capped with MTA. In addition, in order to understand the role of transforming growth factor-beta 1 (TGF-beta 1) during reparative dentinogenesis, the expression of BSP and DSPP mRNA was analyzed by RT-PCR in a human dental pulp cell culture, and the transforming growth factor-beta 1 receptors (T beta RI) and Smad 2/3 were examined by immunofluorescence in an animal model. DSP was expressed in the normal odontoblasts and odontoblast-like cells of the reparative dentin. Interestingly, BSP was strongly expressed in the odontoblast-like cells of reparative dentin. The level of the T beta RI and Smad 2/3 proteins was higher in the reparative dentin than in the normal dentin. TGF-beta 1 up-regulated BSP in the human pulp cell cultures. This suggests that reparative dentin has both dentinogenic and osteogenic characteristics that are mediated by TGF-beta 1.

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