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首页> 外文期刊>Cell metabolism >ATF4-mediated induction of 4E-BP1 contributes to pancreatic beta cell survival under endoplasmic reticulum stress.
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ATF4-mediated induction of 4E-BP1 contributes to pancreatic beta cell survival under endoplasmic reticulum stress.

机译：ATF4介导的4E-BP1诱导在内质网应激下胰腺β细胞存活。

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摘要

Endoplasmic reticulum (ER) stress-mediated apoptosis may play a crucial role in loss of pancreatic beta cell mass, contributing to the development of diabetes. Here we show that induction of 4E-BP1, the suppressor of the mRNA 5' cap-binding protein eukaryotic initiation factor 4E (eIF4E), is involved in beta cell survival under ER stress. 4E-BP1 expression was increased in islets under ER stress in several mouse models of diabetes. The Eif4ebp1 gene encoding 4E-BP1 was revealed to be a direct target of the transcription factor ATF4. Deletion of the Eif4ebp1 gene increased susceptibility to ER stress-mediated apoptosis in MIN6 beta cells and mouse islets, which was accompanied by deregulated translational control. Furthermore, Eif4ebp1 deletion accelerated beta cell loss and exacerbated hyperglycemia in mouse models of diabetes. Thus, 4E-BP1 induction contributes to the maintenance of beta cell homeostasis during ER stress and is a potential therapeutic target for diabetes.
机译：内质网（ER）应激介导的细胞凋亡可能在胰腺β细胞量减少中起关键作用，从而促进了糖尿病的发展。在这里我们显示，诱导4E-BP1，即mRNA 5'帽结合蛋白真核起始因子4E（eIF4E）的抑制剂，参与内质网应激下的β细胞存活。在几种糖尿病小鼠模型中，内质网应激下胰岛中的4E-BP1表达增加。编码4E-BP1的Eif4ebp1基因被发现是转录因子ATF4的直接靶标。 Eif4ebp1基因的删除增加了MIN6 beta细胞和小鼠胰岛对内质网应激介导的细胞凋亡的敏感性，并伴有翻译控制失调。此外，Eif4ebp1缺失加速了糖尿病小鼠模型中的β细胞丢失并加剧了高血糖症。因此，4E-BP1诱导有助于在内质网应激期间维持β细胞稳态，并且是糖尿病的潜在治疗靶标。

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