Neurotensin receptor-2 and-3 are crucial for the anti-apoptotic effect of neurotensin on pancreatic β-TC3 cells

被引：35

作者：

Beraud-Dufour, Sophie ^{[1
]}

Coppola, Thierry ^{[1
]}

Massa, Fabienne ^{[1
]}

Mazella, Jean ^{[1
]}

机构：

[1] Univ Nice Sophia Antipolis, Inst Pharmacol Mol & Cellulaire, CNRS, UMR 6097, F-06560 Valbonne, France

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2009年 / 41卷 / 12期

关键词：

Neurotensin; Receptor; Apoptosis; Beta cell; Receptor complex; CENTRAL-NERVOUS-SYSTEM; NTS3; RECEPTORS; PROTEIN; ROLES; OLIGOMERIZATION; SORTILIN; COMPLEX; GROWTH;

D O I：

10.1016/j.biocel.2009.04.002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The neuropeptide neurotensin (NT) has been recently shown to protect pancreatic beta cells from toxic agents-induced apoptosis through interaction with the NT receptor-2 (NTSR2) and activation of the phosphatidyl inositol-3 kinase pathway. However, expression of the NT receptor-3/sortilin (NTSR3) in the mouse pancreatic beta cell line R-TC3 led us to investigate its possible functional role in these cells. By using siRNA, immunoprecipitation, co-localization and caspase-3 assays, we provide evidence for a functional endogenous interaction between NTSR2 and NTSR3. Expression of both receptors is necessary for the protective action of NT on staurosporine-induced caspase-3 activity in P-TO cells. Moreover, NTSR2 and NTSR3 co-immunoprecipitate and are co-localized at the plasma membrane. Thus, the NT response in beta cells is controlled by the formation of a functional complex between NTSR2 and NTSR3. (C) 2009 Elsevier Ltd. All rights reserved.

引用

页码：2398 / 2402

页数：5

共 18 条

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