Diabetes:Kv2.1集群有助于胰岛素胞外分泌同时可以缓解人类β类细胞功能障碍

2017-06-19 MedSci MedSci原创

胞外分泌胰岛素是由控制兴奋性和Ca2 +涌入的离子通道调控的。这些通道在调控膜质微区结构方面也有重要作用。本次研究中我们探究了INS 832/13细胞和β型细胞中K+ (Kv) 通道Kv2.1 (KCNB1)促进去极化诱发胞外分泌的机制,这些细胞来源于没患和患有2型糖尿病(T2D)的捐赠者。

胞外分泌胰岛素是由控制兴奋性和Ca2 +涌入的离子通道调控的。这些通道在调控膜质微区结构方面也有重要作用。本次研究中我们探究了INS 832/13细胞和β型细胞中K+ (Kv) 通道Kv2.1 (KCNB1)促进去极化诱发胞外分泌的机制,这些细胞来源于没患和患有2型糖尿病(T2D)的捐赠者。我们发现Kv2.1能够在质膜上形成6-12四聚物通道集群促进胰岛素的胞外分泌,而Kv2.2 (KCNB2)却不能。敲低Kv2.1的表达量会减少锚定质膜的分泌颗粒。表达全长的野生型类型的Kv2.1能够支持葡萄糖依赖型的分泌颗粒的招募。但是,一个截短类型的Kv2.1(Kv2.1-ΔC318)依然保持电功能和与突触融合蛋白1A结合功能,却缺乏形成集群的能力,并不提高颗粒招募或胞外分泌能力。在2型糖尿病胰岛中KCNB1的表达确实降低,进一步敲低KCNB1并不能抑制2型糖尿病β型细胞中K+ (Kv)电流。上调表达野生型类型的Kv2.1而不是截短类型的Kv2.1(Kv2.1-ΔC318)能够降低2型糖尿病β型细胞中胞吐的表型,增加2型糖尿病胰岛中胰岛素的分泌。因此,Kv2.1直接促进胰岛素胞外分泌的能力取决于离子通道集群。该通道缺失这种结构性的作用可能导致糖尿病中胰岛素分泌受损。

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    2017-08-10 仁者大医
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    2017-07-15 gwc392
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    2017-07-12 baoya
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