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SUMOylation of Pdia3 exacerbates proinsulin misfolding and ER stress in pancreatic beta cells

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单位： [1]The Center for Biomedical Research, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, China [2]Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Tongji Hospital Research Building, Tongji Hospital, Wuhan, China [3]Clinical Molecular Immunology Center, Department of Immunology, School of Medicine, Yangtze University, Jingzhou 434023, China [4]ULB Center for Diabetes Research, Université Libre de Bruxelles, 808 Route de Lennik, B-1070 Brussels, Belgium [5]Indiana Biosciences Research Institute (IBRI), Indianapolis, IN, USA [6]Diabetes Center, the Second Xiangya Hospital, Institute of Metabolism and Endocrinology, Central South University, Changsha, China [7]Department of Endocrinology and Metabolism, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, China

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关键词： Beta cell ER stress Pdia3 Proinsulin misfolding SUMOylation

摘要：

SUMOylation has long been recognized to regulate multiple biological processes in pancreatic beta cells, but its impact on proinsulin disulfide maturation and endoplasmic reticulum (ER) stress remains elusive. Herein, we conducted comparative proteomic analyses of SUMOylated proteins in primary mouse/human islets following proinflammatory cytokine stimulation. Cytokine challenge rendered beta cells to undergo a SUMOylation turnover manifested by the changes of SUMOylation substrates and SUMOylation levels for multiple substrates. Our data support that SUMOylation may play a crucial role to regulate proinsulin misfolding and ER stress at least by targeting Protein Disulfide Isomerase a3 (Pdia3). SUMOylation regulates Pdia3 enzymatic activity, subcellular localization, and protein binding ability. Furthermore, SUMOylation of Pdia3 exacerbated proinsulin misfolding and ER stress, and repressed Stat3 activation. In contrast, disruption of Pdia3 SUMOylation markedly rescued the outcomes. Collectively, our study expands the understanding how SUMOylation regulates ER stress in beta cells, which shed light on developing potential strategies against beta cell dysfunction.

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出版当年[2019]版：

大类 | 2 区医学

小类 | 2 区遗传学 2 区医学：研究与实验

最新[2025]版：

大类 | 3 区医学

小类 | 3 区遗传学 3 区医学：研究与实验

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出版当年[2018]版：

Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q1 GENETICS & HEREDITY

最新[2024]版：

Q1 GENETICS & HEREDITY Q2 MEDICINE, RESEARCH & EXPERIMENTAL

影响因子： 4.2 最新[2024版] 4.7 最新五年平均 4.746 出版当年[2018版] 5.114 出版当年五年平均 4.938 出版前一年[2017版] 4.427 出版后一年[2019版]

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第一作者单位： [1]The Center for Biomedical Research, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, China

通讯作者：

通讯机构： [1]The Center for Biomedical Research, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, China [2]Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Tongji Hospital Research Building, Tongji Hospital, Wuhan, China

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