期刊
JOURNAL OF PROTEOME RESEARCH
卷 14, 期 2, 页码 688-699出版社
AMER CHEMICAL SOC
DOI: 10.1021/pr500643h
关键词
Diabetes; oxidative stress; ER stress; inflammation; 2D-DIGE; MALDI-TOF MS
资金
- Juvenile Diabetes Research Foundation International [17-2012-134]
- Australian National Health and Medical Research Council
- Marie Curie Fellowship from the European Union [CONBIOS 330486]
- Melbourne Research Unit for Facial Disorders
The complex interplay of many cell types and the temporal heterogeneity of pancreatic islet composition obscure the direct role of resident alpha and beta cells in the development of Type 1 diabetes. Therefore, in addition to studying islets isolated from non-obese diabetic mice, we analyzed homogeneous cell populations of murine alpha (alpha TC-1) and beta (NIT-1) cell lines to understand the role and differential survival of these two predominant islet cell populations. A total of 56 proteins in NIT-1 cells and 50 in alpha TC-1 cells were differentially expressed when exposed to proinflammatory cytokines. The major difference in the protein expression between cytokine-treated NIT-1 and alpha TC-1 cells was free radical scavenging enzymes. A similar observation was made in cytokine-treated whole islets, where a comprehensive analysis of subcellular fractions revealed that 438 unique proteins were differentially expressed under inflammatory conditions. Our data indicate that beta cells are relatively susceptible to ER and oxidative stress and reveal key pathways that are dysregulated in beta cells during cytokine exposure. Additionally, in the islets, inflammation also leads to enhanced antigen presentation, which completes a three-way insult on beta cells, rendering them targets of infiltrating T lymphocytes.
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