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首页> 外文期刊>Cell metabolism >The complement inhibitor CD59 regulates insulin secretion by modulating exocytotic events
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The complement inhibitor CD59 regulates insulin secretion by modulating exocytotic events

机译：补体抑制剂CD59通过调节胞吐事件来调节胰岛素分泌

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摘要

Type 2 diabetes is triggered by reduced insulin production, caused by genetic and environmental factors such as inflammation originating from the innate immune system. Complement proteins are a component of innate immunity and kill non-self cells by perforating the plasma membrane, a reaction prevented by CD59. Human pancreatic islets express CD59 at very high levels. CD59 is primarily known as a plasma membrane protein in membrane rafts, but most CD59 protein in pancreatic β cells is intracellular. Removing extracellular CD59 disrupts membrane rafts and moderately stimulates insulin secretion, whereas silencing intracellular CD59 markedly suppresses regulated secretion by exocytosis, as demonstrated by TIRF imaging. CD59 interacts with the exocytotic proteins VAMP2 and Syntaxin-1. CD59 expression is reduced by glucose and in rodent diabetes models but upregulated in human diabetic islets, potentially reflecting compensatory reactions. This unconventional action of CD59 broadens the established view of innate immunity in type 2 diabetes.
机译：2型糖尿病是由胰岛素产生减少引起的，胰岛素产生是由遗传和环境因素引起的，例如先天免疫系统引起的炎症。补体蛋白是先天免疫的组成部分，可通过穿刺质膜来杀死非自身细胞，这种反应被CD59阻止。人胰岛以非常高的水平表达CD59。 CD59在膜筏中主要被称为质膜蛋白，但胰腺β细胞中的大多数CD59蛋白在细胞内。如TIRF成像所示，去除细胞外CD59可破坏膜筏并适度刺激胰岛素分泌，而沉默细胞内CD59可显着抑制胞吐作用调节分泌。 CD59与胞吐蛋白VAMP2和Syntaxin-1相互作用。葡萄糖和啮齿类糖尿病模型中CD59的表达降低，但在人类糖尿病胰岛中CD59的表达上调，这可能反映了代偿反应。 CD59的这种非常规作用拓宽了2型糖尿病先天免疫的既定视野。

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