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对两种富含亮氨酸的小分子蛋白聚糖(双糖链蛋白聚糖和核心蛋白聚糖)的靶向破坏,对釉质和牙本质形成产生了不同的影响。

Targeted disruption of two small leucine-rich proteoglycans, biglycan and decorin, excerpts divergent effects on enamel and dentin formation.

作者信息

Goldberg M, Septier D, Rapoport O, Iozzo R V, Young M F, Ameye L G

机构信息

Laboratoire: Réparation et Remodelage des Tissus Oro-Faciaux, EA 2496, Groupe Matrices Extracellulaires et Minéralisations, Faculté de Chirurgie Dentaire, Université Paris V, Montrouge, 92120, France.

出版信息

Calcif Tissue Int. 2005 Nov;77(5):297-310. doi: 10.1007/s00223-005-0026-7. Epub 2005 Nov 5.

Abstract

Small leucine-rich proteoglycans have been suggested to affect mineralization of dental hard tissues. To determine the functions of two of these small proteoglycans during the early stages of tooth formation, we characterized the dental phenotypes of biglycan (BGN KO) and decorin deficient (DCN KO) mice and compared them to that of wild type mice. Each targeted gene disruption resulted in specific effects on dentin and enamel formation. Dentin was hypomineralized in both knock out mice, although the effect was more prominent in the absence of decorin. Enamel formation was dramatically increased in newborn biglycan knockout mice but delayed in absence of decorin. Increased enamel formation in the former case resulted from an upregulation of amelogenin synthesis whereas delayed enamel formation in the later case was most probably an indirect consequence of the high porosity of the underlying dentin. Enamelin expression was unchanged in BGN KO, and reduced in DCN KO. Dentin sialoprotein (DSP), a member of the family of phosphorylated extracellular matrix proteins that play a role in dentinogenesis, was overexpressed in BGN-KO odontoblasts and in the sub-odontoblastic layer. In contrast, a decreased expression of DSP was detected in DCN KO. Dentin matrix protein-1 (DMP-1), bone sialoprotein (BSP) and osteopontin (OPN) were upregulated in BGN KO and downregulated in the DCN KO. Despite the strong effects induced by these deficiencies in newborn mice, no significant difference was detected between the three genotypes in adult mice, suggesting that the effects reported here in newborn mice are transient and subjected to self-repair.

摘要

富含亮氨酸的小分子蛋白聚糖被认为会影响牙齿硬组织的矿化。为了确定其中两种小分子蛋白聚糖在牙齿形成早期阶段的功能,我们对双糖链蛋白聚糖缺陷(BGN KO)和核心蛋白聚糖缺陷(DCN KO)小鼠的牙齿表型进行了表征,并将它们与野生型小鼠进行了比较。每种靶向基因破坏对牙本质和釉质形成都产生了特定影响。两种敲除小鼠的牙本质矿化不足,尽管在缺乏核心蛋白聚糖时这种影响更为明显。新生双糖链蛋白聚糖敲除小鼠的釉质形成显著增加,但在缺乏核心蛋白聚糖时则延迟。前一种情况下釉质形成增加是由于釉原蛋白合成上调,而后一种情况下釉质形成延迟很可能是下层牙本质高孔隙率的间接结果。釉蛋白在BGN KO中表达不变,在DCN KO中表达降低。牙本质涎蛋白(DSP)是在牙本质形成中起作用的磷酸化细胞外基质蛋白家族的成员,在BGN-KO成牙本质细胞和亚成牙本质层中过表达。相反,在DCN KO中检测到DSP表达降低。牙本质基质蛋白-1(DMP-1)、骨涎蛋白(BSP)和骨桥蛋白(OPN)在BGN KO中上调,在DCN KO中下调。尽管这些缺陷在新生小鼠中产生了强烈影响,但在成年小鼠的三种基因型之间未检测到显著差异,这表明此处报道的新生小鼠中的影响是短暂的且可自我修复。

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