交界上皮细胞与马拉色斯上皮细胞间的发育关系

Shubo Li, Shufang Li, Mingguo Cao
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摘要

角蛋白 17(K17)被认为是受淋巴增强因子-1(Lef-1)调控的候选靶基因。K17 是区分交界上皮(JE)和马拉色斯上皮休止期(ERM)的标记。然而,在这种情况下,Lef-1 与 K17 的关系并不明确。此外,其他角蛋白如 K5、K6、K7 和 K16 的表达也未见报道。因此,我们的研究旨在检测 K5、K6、K7、K14、K16、K17 和 Lef-1 在出生后发育牙齿中的表达,并明确 JE 和 ERM 的相应免疫表型。使用出生后(PN)第 3.5 天至 PN21 天的 Wistar 大鼠的上颚并对其进行免疫组化处理。K5 和 K14 在内侧釉质上皮(IEE)、还原釉质上皮(REE)、ERM 和 JE 中强烈表达。除了口腔上皮的强染色外,组织中没有 K16 的染色。具体来说,在 PN3.5 和 PN7 时,K17 最初在 IEE 中强表达,随后呈阴性。在 PN16 和 PN21,REE 和 ERM 中的 K17 均呈强染色,而 JE 中的 K17 则呈阴性。此外,K6、K7 和 Lef-1 在所调查的任何组织中均未检测到。REE 和 ERM 在糜烂前的角蛋白表达模式相同,而 JE 在糜烂后的 K17 表达与 ERM 不同。K17 的表达与 Lef-1 的表达不一致。这些数据表明,JE具有不同于ERM的独特表型,而ERM是牙源性的。
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Developmental relationship between junctional epithelium and epithelial rests of Malassez.

Keratin 17 (K17) is thought to be a candidate target gene for regulation by Lymphoid Enhancer Factor-1 (Lef-1). K17 is a marker that distinguishes junctional epithelium (JE) from epithelial rests of Malassez (ERM). However, the relationship of Lef-1 to K17 is not clear in this context. Moreover, the expression of other keratins such as K5, K6, K7 and K16 is not reported. Therefore, the aim of our study was to assay the expression of K5, K6, K7, K14, K16, K17 and Lef-1 in postnatal developing teeth, and clarify the corresponding immunophenotypes of the JE and ERM. Upper jaws of Wistar rats aged from postnatal (PN) day 3.5 to PN21 were used and processed for immunohistochemistry. K5 and K14 were intensely expressed in inner enamel epithelium (IEE), reduced enamel epithelium (REE), ERM and JE. There was no staining for K16 in the tissue, except for strong staining in the oral epithelium. Specifically, at PN3.5 and PN7, K17 was initially strongly expressed and then negative in the IEE. At PN16 and PN21, both REE and ERM were strongly stained for K17, whereas K17 was negative in the JE. In addition, K6, K7 and Lef-1 were not detected in any tissue investigated. REE and ERM have an identical keratin expression pattern before eruption, while JE differs from ERM in the expression of K17 after eruption. The expression of K17 does not coincide with that of Lef-1. These data indicate that JE has a unique phenotype different from ERM, which is of odontogenic origin.

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