Upregulation of GRP78 is accompanied by decreased antioxidant response and mitophagy promotion in streptozotocin-induced type 1 diabetes in rats - original data

Endoplasmic reticulum stress, oxidative stress, and mitochondrial dysfunction are interconnected processes involved in the pathogenesis of diabetes mellitus (DM). In the present study, we demonstrate a distinct unfolded protein response (UPR) signaling pathways in two mammalian models of DM: β-TC-6 cell line and streptozotocin induced type 1 diabetes model in rats. However, a feature common to both systems was the upregulation of the GRP78 protein. Moreover, in vivo studies showed the disruption of the antioxidant system and an escalation of mitophagy against the background of a depletion of the level of ATP in pancreatic cells. In conclusion, we suggest that glucotoxic conditions induced GRP78 upregulation, and next cause depletion of the antioxidant pool and disruption of the functioning of antioxidant defense enzymes and in consequence promote mitophagy in pancreatic cells. Therefore, GRP78 may be considered as a potential therapeutic factor in patients with diabetes.

Description

Raw data in a xlsx file: Original data used to generate the presentation of results in the figure 1-4.

Keywords

Diabetes mellitus, Endoplasmic reticulum stress, Mitophagy, Oxidative stress, GRP78

URI

https://rdb.ur.edu.pl/handle/item/52

Research funding institutions

This work was supported by the National Science Centre of Poland, Miniatura 5, Grant number: 2021/05/X/NZ3/01000.

Collections

Instytut Biotechnologii / Institute of Biotechnology

Type

raw dataset

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