The core autophagy protein ATG5 controls the polarity of the Golgi apparatus and insulin secretion of pancreatic beta cells.
The core autophagy protein ATG5 controls the polarity of the Golgi apparatus and insulin secretion of pancreatic beta cells.
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DOI：
10.1016/j.bbrc.2022.08.084
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发表时间：
2022-09
影响因子：
3.1
通讯作者：
Xintong Pei;Huiyu Wang;P. Xu;Kuo Liang;Lin Yuan
中科院分区：
文献类型：
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作者：
Xintong Pei;Huiyu Wang;P. Xu;Kuo Liang;Lin Yuan
胰腺β细胞是胰岛中结构和功能极化的胰岛素产生细胞。高尔基复合体的组织和位置在维持极化细胞状态中起着关键作用，但决定胰腺β细胞高尔基极化的因素和分子机制仍然未知。在目前的研究中，使用胰腺β细胞特异性Atg5敲除小鼠，我们发现Atg5，一个自噬的必需基因，通过影响参与囊泡运输的基因的表达，在调节高尔基体的完整性和极化中起着关键作用。Atg5的缺失导致内质网（ER）应激并损害胰岛素原的分布和胰腺β细胞的胰岛素分泌，这进一步加重糖尿病。这些结果有助于全面了解自噬介导的高尔基体极化及其对胰腺β细胞功能的调节。
Pancreatic beta cells are insulin-producing cells that are structurally and functionally polarized in the islets of Langerhans. The organization and position of the Golgi complex play a key role in maintaining a polarized cell state, but the factors and molecular mechanisms determining the Golgi polarization of pancreatic beta cells are still unknown. In the current study, using pancreatic beta cell-specificAtg5knockout mice, we found thatAtg5, an essential gene for autophagy, plays a pivotal role in regulating Golgi integrity and polarization by affecting the expression of genes involved in vesicle transport. Deletion ofAtg5led to endoplasmic reticulum (ER) stress and impaired the distribution of proinsulin and insulin secretion of pancreatic beta cells, which further exacerbates diabetes. These results contribute to a comprehensive understanding of autophagy-mediated Golgi polarization and its regulation of the function of pancreatic beta cells.