突触结合蛋白IV调节LbetaT2细胞中致密核心囊泡（DCV）的释放。

Synaptotagmin IV regulates dense core vesicle (DCV) release in LbetaT2 cells.

作者信息

Hu Zhi-Tao, Chen Mao-Rong, Ping Zhao, Dong Yong-Ming, Zhang Rong-Ying, Xu Tao, Wu Zheng-Xing

机构信息

Key Laboratory of Molecular Biophysics, Ministry of Education, and Joint Laboratory of Institute of Biophysics & Huazhong University of Science and Technology, Huazhong University of Science and Technology, Luoyu Road 1037#, Wuhan 430074, PR China.

出版信息

Biochem Biophys Res Commun. 2008 Jul 11;371(4):781-6. doi: 10.1016/j.bbrc.2008.04.174. Epub 2008 May 9.

DOI:10.1016/j.bbrc.2008.04.174

PMID:18468511

Abstract

Synaptotagmins (Syts) are calcium-binding proteins which are conserved from nematodes to humans. Fifteen Syts have been identified in mammalian species. Syt I is recognized as a Ca(2+) sensor for the synchronized release of synaptic vesicles in some types of neurons, but its role in the secretion of dense core vesicles (DCVs) remains unclear. The function of Syt IV is of particular interest because it is rapidly up-regulated by chronic depolarization and seizures. Using RNAi-mediated gene silencing, we have explored the role of Syt I and IV on secretion in a pituitary gonadotrope cell line. Downregulation of Syt IV clearly reduced Ca(2+)-triggered exocytosis of dense core vesicles (DCVs) in LbetaT2 cells. Syt I silencing, however, had no effect on vesicular release.

摘要

突触结合蛋白（Syts）是一类钙结合蛋白，从线虫到人类都保守存在。在哺乳动物物种中已鉴定出15种突触结合蛋白。在某些类型的神经元中，突触结合蛋白I被认为是用于同步释放突触小泡的Ca(2+)传感器，但其在致密核心囊泡（DCV）分泌中的作用仍不清楚。突触结合蛋白IV的功能特别受关注，因为它会被慢性去极化和癫痫发作快速上调。利用RNAi介导的基因沉默技术，我们探究了突触结合蛋白I和IV在垂体促性腺激素细胞系分泌中的作用。突触结合蛋白IV的下调明显降低了LbetaT2细胞中Ca(2+)触发的致密核心囊泡（DCV）胞吐作用。然而，沉默突触结合蛋白I对囊泡释放没有影响。