Store-operated Ca2+ entry: a key component of the insulin secretion machinery

被引:16
作者
Sabourin, Jessica [1 ]
Allagnat, Florent [2 ]
机构
[1] Fac Pharm Chatenay Malabry, INSERM, UMR S 1180, Signalisat & Physiopathol Cardiovasc,LabEx LERMIT, Chatenay Malabry, France
[2] CHU Vaudois, Dept Vasc Surg, Lausanne, Switzerland
基金
瑞士国家科学基金会;
关键词
store-operated Ca2+ entry; TRPC1; STIM1; Orai1; insulin secretion; pancreatic beta-cells; PANCREATIC BETA-CELLS; TRPC CHANNELS; CALCIUM-ENTRY; SMOOTH-MUSCLE; STIM1; INFLUX; ORAI1;
D O I
10.1530/JME-16-0106
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Normal plasma glucose level is ensured by the action of insulin, the major hypoglycemic hormone. Therefore, it is not surprising that insulin release from pancreatic beta-cells of the islets of Langerhans is controlled by an array of balanced mechanisms in which glucose plays the leading role. Glucose triggers insulin secretion through the well-described pathway of ATP-driven closure of ATP-sensitive potassium channels (K-ATP), depolarization of the plasma membrane, and opening of the voltage-dependent Ca2+ channels ( VDCC). The subsequent rapid rise in cytoplasmic free Ca2+ concentration triggers insulin exocytosis. However, despite more than 40 years of investigation, certain aspects of the intracellular Ca2+ responses to glucose and secretagogues remain unexplained, suggesting the involvement of additional Ca2+ channels. Here, we discuss the emerging role of store-operated Ca2+ channels carried by Orai1 and transient receptor potential canonical 1 (TRPC1) proteins and regulated by the stromal interaction molecule 1 (STIM1) in the control of glucose-induced insulin secretion. The role of other voltage-independent cation channels formed by other members of the TRP channels family is also addressed.
引用
收藏
页码:F35 / F39
页数:5
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