GSTO1 regulates insulin biosynthesis in pancreatic β cells

被引：6

作者：

Wang, Linlin ^{[1
,2
]}

Lei, Lei ^{[3
]}

Xu, Tao ^{[1
,2
]}

Wang, You ^{[1
]}

机构：

[1] Chinese Acad Sci, CAS Ctr Excellence Biomacromol, Inst Biophys, Natl Lab Biomacromol, Beijing 100101, Peoples R China

[2] Univ Chinese Acad Sci, Coll Life Sci, Beijing 100049, Peoples R China

[3] Chinese Acad Med Sci, Peking Union Med Coll, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Beijing 100050, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2020年 / 524卷 / 04期

关键词：

GSTO1; Pancreatic beta cell; Insulin biosynthesis; PDX1; Diabetes; GLUTATHIONE-S-TRANSFERASE; OMEGA-CLASS; METABOLISM; SECRETION; GENE; IDENTIFICATION; CHANNEL; ISLETS; FAMILY; ONSET;

D O I：

10.1016/j.bbrc.2020.01.151

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Insulin biosynthesis and secretion by pancreatic beta cells are critical for the maintenance of blood glucose homeostasis. Here, we show that the expression of glutathione S-transferase omega-1 (GSTO1) is upregulated in the primary islet cells of diabetic Goto-Kakizaki (GK) rats. Knocking out GSTO1 upregulated insulin transcripts and increased the insulin content in both INS-1 cells and primary islet cells. In contrast, overexpression of GSTO1 reduced the insulin content. Furthermore, knocking out GSTO1 increased the expression of pancreatic duodenal homeobox-1 (PDX1) at both the transcription and protein levels. These results indicate that GSTO1 may be involved in the regulation of insulin biosynthesis by modulating the transcriptional expression of PDX1. (C) 2020 Elsevier Inc. All rights reserved.

引用

页码：936 / 942

页数：7

共 34 条

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