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HNK-1碳水化合物表位及其合成葡糖醛酸基转移酶基因在大鼠神经嵴细胞迁移中的作用

Roles of HNK-1 carbohydrate epitope and its synthetic glucuronyltransferase genes on migration of rat neural crest cells.

作者信息

Nagase Takashi, Sanai Yutaka, Nakamura Shun, Asato Hirotaka, Harii Kiyonori, Osumi Noriko

机构信息

Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.

出版信息

J Anat. 2003 Jul;203(1):77-88. doi: 10.1046/j.1469-7580.2003.00205.x.

Abstract

HNK-1 carbohydrate epitope is localized on the surface of avian neural crest cells (NCCs), and is necessary for their migration. However, it is still disputed whether the epitope works in similar ways in mammalian embryos. In this study, we found that HNK-1 carbohydrate epitope was specifically detected in some of the cranial ganglia, migrating trunk NCCs and some non-NCC derivatives in the rat embryo. Two genes encoding glucuronyltransferases that synthesize the HNK-1 epitope in vitro (GlcAT-P and GlcAT-D) were recently identified in the rat. Interestingly, the NCCs in the cranial ganglia expressed the GlcAT-D gene, whereas the migrating trunk NCCs expressed the GlcAT-P gene. To investigate in vivo functions of the GlcATs in the NCC migration further, we overexpressed GlcAT genes by electroporation in the cranial NCCs in cultured rat embryos. Transfection of both GlcAT genes resulted in efficient synthesis of the HNK-1 epitope in the NCCs. GlcAT-P overexpression increased distance of cranial NCC migration, whereas GlcAT-D overexpression did not show this effect. Our data suggest that the HNK-1 epitope synthesized by different GlcATs is involved in migration in the sublineages of the NCCs in the rat embryo, and that GlcAT-P and GlcAT-D mediate different effects on the NCC migration.

摘要

HNK-1碳水化合物表位定位于禽类神经嵴细胞(NCCs)表面,是其迁移所必需的。然而,该表位在哺乳动物胚胎中是否以类似方式起作用仍存在争议。在本研究中,我们发现HNK-1碳水化合物表位在大鼠胚胎的一些颅神经节、迁移的躯干NCCs和一些非NCC衍生物中被特异性检测到。最近在大鼠中鉴定出两个在体外合成HNK-1表位的编码葡萄糖醛酸基转移酶的基因(GlcAT-P和GlcAT-D)。有趣的是,颅神经节中的NCCs表达GlcAT-D基因,而迁移的躯干NCCs表达GlcAT-P基因。为了进一步研究GlcATs在NCC迁移中的体内功能,我们通过电穿孔在培养的大鼠胚胎的颅NCCs中过表达GlcAT基因。两种GlcAT基因的转染导致NCCs中HNK-1表位的有效合成。GlcAT-P的过表达增加了颅NCC迁移的距离,而GlcAT-D的过表达未显示出这种效果。我们的数据表明,由不同GlcATs合成的HNK-1表位参与大鼠胚胎NCCs亚系中的迁移,并且GlcAT-P和GlcAT-D对NCC迁移介导不同的作用。

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