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增加的赫索胺生物合成路径流量会改变INS-1E细胞和小鼠群岛的细胞-细胞粘附

Dario Domenico Lofrumento¹, Alessandro Miraglia¹, Velia La Pesa²

¹DiSTeBA, Centro Ecotekne, Strada Monteroni, University of Salento, 73100, Lecce, Italy.

|June 12, 2023

概括

增加的六胺通路流量会通过改变E-cadherin的局部化而损害β细胞相互作用,影响细胞粘附和岛屿结构. 这揭示了在2型糖尿病中控制葡萄糖毒性的新目标.

科学领域:

内分泌学在内分泌学.
细胞生物学细胞生物学
糖尿病研究糖尿病研究

背景情况:

2型糖尿病涉及β细胞衰竭,其特征是亡和功能障碍.
与赫索胺生物合成途径相关的葡萄糖毒性,有助于β细胞死亡.
贝塔细胞通信 (同型相互作用) 对胰岛素分泌和小岛功能至关重要.

研究的目的:

为了研究如何增加赫索胺生物合成途径的流量影响β细胞-β细胞相互作用.
确定E-cadherin和β-catenin在调解这些效应中的作用.
探索葡萄糖毒性诱导的β细胞功能障碍的潜在治疗点.

主要方法:

在实验中利用了INS-1E细胞和小鼠群岛.
评估了E-cadherin和β-catenin的表达和局部化,通过免疫光学,免疫组织化学和西部斑.
通过显微观观测,通过悬浮滴聚合试验和小岛架构评估细胞-细胞粘附.

主要成果:

增加的六胺通路流量导致细胞表面E-cadherin减少和细胞内E-cadherin增加,从戈尔吉到ER的局部性改变.
β-catenin从血转移到细胞质中,反映了E-cadherin的变化.
在INS-1E细胞中,聚合率降低,而ex vivo岛屿显示结构改变和表面减少E-cadherin/β-catenin.

结论:

升高的六胺通路流动会破坏β细胞中的E-cadherin定位,损害细胞-细胞粘附和岛屿形态.
在E-cadherin功能中的这些变化代表了一种新的机制,有助于葡萄糖毒性.
针对这些E-cadherin介导的变化提供了一种潜在的策略,以减轻2型糖尿病中的β细胞损伤.

关键词:

这是E-cadherin.穆林岛屿的小岛屿胰腺β细胞 - - 胰腺β细胞

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