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牙本质基质蛋白与牙本质形成

Dentin matrix proteins and dentinogenesis.

作者信息

Butler W T

机构信息

University of Texas--Houston, Health Science Center, Dental Branch 77030, USA.

出版信息

Connect Tissue Res. 1995;33(1-3):59-65. doi: 10.3109/03008209509016983.

DOI:10.3109/03008209509016983
PMID:7554963
Abstract

The precise mechanisms involved in dentinogenesis are not understood; however, the information to date suggests that a number of highly controlled extracellular events are involved. Mature odontoblasts secrete collagen at the cell border into predentin. They synthesize and secrete other non-collagenous proteins (NCPs) at the mineralization front, possibly through odontoblastic processes. A collagen-NCP complex is formed at the predentin-dentin border and apatite crystal initiation and growth takes place. One of the research needs is to uncover the nature of this dentin collagen-NCP complex and to understand how it controls mineralization. At least three dentin specific NCPs are known: phosphophoryn(s), dentin sialoprotein (DSP) and AG1 (Dmp1). Other macromolecules are commonly made by osteoblasts and odontoblasts and participate in bone and dentin formation. Some progress in understanding dentin mineralization has been gained by focusing upon the role of phosphophoryns. These highly phosphorylated proteins are secreted at the mineralization front, where a small portion binds in the gap region of type I collagen fibrils. This portion of phosphoproteins probably initiates formation of plate-like apatite crystals. Additional phosphoryns in higher concentrations bind to the growing apatite crystals and slow their growth, possibly influencing their size and shape. Other areas which need careful investigations are those involving the mechanisms involved in odontoblast differentiation, how the synthesis of the dentin specific NCPs is controlled and the precise roles of these macromolecules in dentinogenesis. Future experimentation will focus on the gene structures for these NCPs and the mechanisms of tissue specific gene regulation.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

牙本质形成所涉及的精确机制尚不清楚;然而,迄今为止的信息表明,这一过程涉及许多受到高度调控的细胞外事件。成熟的成牙本质细胞在细胞边界处将胶原蛋白分泌到前期牙本质中。它们可能通过成牙本质细胞突起在矿化前沿合成并分泌其他非胶原蛋白(NCPs)。在前期牙本质 - 牙本质边界处形成胶原蛋白 - NCP复合物,磷灰石晶体开始形成并生长。其中一项研究需求是揭示这种牙本质胶原蛋白 - NCP复合物的性质,并了解其如何控制矿化。已知至少有三种牙本质特异性NCPs:磷酸化磷蛋白、牙本质涎蛋白(DSP)和AG1(Dmp1)。其他大分子通常由成骨细胞和成牙本质细胞产生,并参与骨和牙本质的形成。通过关注磷酸化磷蛋白的作用,在理解牙本质矿化方面取得了一些进展。这些高度磷酸化的蛋白质在矿化前沿分泌,其中一小部分结合在I型胶原纤维的间隙区域。这部分磷蛋白可能启动片状磷灰石晶体的形成。更高浓度的其他磷酸化磷蛋白与生长中的磷灰石晶体结合并减缓其生长,可能影响其大小和形状。其他需要仔细研究的领域包括成牙本质细胞分化所涉及的机制、牙本质特异性NCPs的合成是如何被控制的以及这些大分子在牙本质形成中的精确作用。未来的实验将集中在这些NCPs的基因结构以及组织特异性基因调控的机制上。(摘要截选至250词)

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