肉毒杆菌神经毒素C1轻链的瞬时表达可差异性抑制克隆β细胞中钙和葡萄糖诱导的胰岛素分泌。

Transient expression of botulinum neurotoxin C1 light chain differentially inhibits calcium and glucose induced insulin secretion in clonal beta-cells.

作者信息

Land J, Zhang H, Vaidyanathan V V, Sadoul K, Niemann H, Wollheim C B

机构信息

Département de Médecine Interne, Centre Médical Universitaire, Université de Genève, Geneva, Switzerland.

出版信息

FEBS Lett. 1997 Dec 8;419(1):13-7. doi: 10.1016/s0014-5793(97)01411-7.

DOI:10.1016/s0014-5793(97)01411-7

PMID:9426210

Abstract

We have investigated the effect of botulinum neurotoxin (BoNT) C1 light chain (LC) on insulin exocytosis from the clonal beta-cell line HIT-T15. In streptolysin-O permeabilized cells, the beta-cell impermeant BoNT C1 cleaved mainly syntaxin 1 and inhibited Ca2+ as well as GTPgammaS induced exocytosis. To study the effect of BoNTs in intact cells, we transiently coexpressed the BoNT LC together with a reporter gene for insulin release. BoNT C1 inhibited K+ induced insulin secretion by 95% but reduced insulin release stimulated by glucose only by 25%. Thus a component of glucose stimulated insulin release is insensitive to BoNT C1.

摘要

我们研究了肉毒杆菌神经毒素（BoNT）C1轻链（LC）对克隆β细胞系HIT-T15胰岛素胞吐作用的影响。在经链球菌溶血素-O通透处理的细胞中，β细胞不透性的BoNT C1主要切割 syntaxin 1，并抑制Ca2+以及GTPγS诱导的胞吐作用。为了研究BoNTs在完整细胞中的作用，我们将BoNT LC与胰岛素释放报告基因一起瞬时共表达。BoNT C1将K+诱导的胰岛素分泌抑制了95%，但仅将葡萄糖刺激的胰岛素释放减少了25%。因此，葡萄糖刺激胰岛素释放的一个组成部分对BoNT C1不敏感。