Abstract:
BACKGROUND:Type 1 diabetes (T1D) is an autoimmune disease in which pancreatic β-cells are destroyed by infiltrating immune cells. Bilateral cooperation of pancreatic β-cells and immune cells has been proposed in the progression of T1D, but as yet no systems study has investigated this possibility. The aims of the study were to elucidate the underlying molecular mechanisms and identify key genes associated with T1D risk using a network biology approach. METHODS:Interactome (protein-protein interaction [PPI]) and transcriptome data were integrated to construct networks of differentially expressed genes in peripheral blood mononuclear cells (PBMCs) and pancreatic β-cells. Centrality, modularity, and clique analyses of networks were used to get more meaningful biological information. RESULTS:Analysis of genes expression profiles revealed several cytokines and chemokines in β-cells and their receptors in PBMCs, which is supports the dialogue between these two tissues in terms of PPIs. Functional modules and complexes analysis unraveled most significant biological pathways such as immune response, apoptosis, spliceosome, proteasome, and pathways of protein synthesis in the tissues. Finally, Y-box binding protein 1 (YBX1), SRSF protein kinase 1 (SRPK1), proteasome subunit alpha1/ 3, (PSMA1/3), X-ray repair cross complementing 6 (XRCC6), Cbl proto-oncogene (CBL), SRC proto-oncogene, non-receptor tyrosine kinase (SRC), phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1), phospholipase C gamma 1 (PLCG1), SHC adaptor protein1 (SHC1) and ubiquitin conjugating enzyme E2 N (UBE2N) were identified as key markers that were hub-bottleneck genes involved in functional modules and complexes. CONCLUSIONS:This study provide new insights into network biomarkers that may be considered potential therapeutic targets.
journal_name
J Diabetesjournal_title
Journal of diabetesauthors
Safari-Alighiarloo N,Taghizadeh M,Tabatabaei SM,Shahsavari S,Namaki S,Khodakarim S,Rezaei-Tavirani Mdoi
10.1111/1753-0407.12483subject
Has Abstractpub_date
2017-08-01 00:00:00pages
764-777issue
8eissn
1753-0393issn
1753-0407journal_volume
9pub_type
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pub_type: 杂志文章,评审
doi:10.1111/j.1753-0407.2010.00090.x
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abstract::Pancreatic β-cells secrete insulin when blood glucose levels become high; however, when β-cells are chronically exposed to hyperglycemia, β-cell function gradually deteriorates, which is known as β-cell glucose toxicity. In the diabetic state, nuclear expression of the pancreatic transcription factors pancreatic and d...
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pub_type: 杂志文章,评审
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journal_title:Journal of diabetes
pub_type: 杂志文章
doi:10.1111/1753-0407.12310
更新日期:2016-05-01 00:00:00
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更新日期:2017-05-01 00:00:00
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pub_type: 杂志文章
doi:10.1111/j.1753-0407.2009.00048.x
更新日期:2010-03-01 00:00:00
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doi:10.1111/1753-0407.12823
更新日期:2018-12-01 00:00:00
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doi:10.1111/j.1753-0407.2010.00066.x
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doi:10.1111/1753-0407.12549
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doi:10.1111/1753-0407.12261
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pub_type: 杂志文章
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更新日期:2020-03-01 00:00:00
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pub_type: 杂志文章
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journal_title:Journal of diabetes
pub_type: 杂志文章,随机对照试验
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更新日期:2018-08-01 00:00:00
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journal_title:Journal of diabetes
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更新日期:2013-12-01 00:00:00
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更新日期:2016-09-01 00:00:00
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journal_title:Journal of diabetes
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更新日期:2009-12-01 00:00:00
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更新日期:2017-03-01 00:00:00