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Abedi M, Gheisari Y. Nodes with high centrality in protein interaction networks are responsible for driving signaling pathways in diabetic nephropathy. PeerJ. 2015;3:e1284doi: 10.7717/peerj.1284.
Abedi, M., & Gheisari, Y. (2015). Nodes with high centrality in protein interaction networks are responsible for driving signaling pathways in diabetic nephropathy. PeerJ, 3e1284. https://doi.org/10.7717/peerj.1284
Abedi, Maryam, and Gheisari, Yousof. "Nodes with high centrality in protein interaction networks are responsible for driving signaling pathways in diabetic nephropathy." PeerJ vol. 3 (2015): e1284. doi: https://doi.org/10.7717/peerj.1284
Abedi M, Gheisari Y. Nodes with high centrality in protein interaction networks are responsible for driving signaling pathways in diabetic nephropathy. PeerJ. 2015 Oct 01;3:e1284. doi: 10.7717/peerj.1284. eCollection 2015. PMID: 26557424; PMCID: PMC4636410.
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PeerJ. 2015 Oct 01;3:e1284. doi: 10.7717/peerj.1284. eCollection 2015.

Nodes with high centrality in protein interaction networks are responsible for driving signaling pathways in diabetic nephropathy.

PeerJ

Maryam Abedi, Yousof Gheisari

Affiliations

  1. Department of Genetics and Molecular Biology, Isfahan University of Medical Sciences , Isfahan , Iran.
  2. Department of Genetics and Molecular Biology, Isfahan University of Medical Sciences , Isfahan , Iran ; Regenerative Medicine Lab, Isfahan Kidney Diseases Research Center, Isfahan University of Medical Sciences , Isfahan , Iran.

PMID: 26557424 PMCID: PMC4636410 DOI: 10.7717/peerj.1284

Abstract

In spite of huge efforts, chronic diseases remain an unresolved problem in medicine. Systems biology could assist to develop more efficient therapies through providing quantitative holistic sights to these complex disorders. In this study, we have re-analyzed a microarray dataset to identify critical signaling pathways related to diabetic nephropathy. GSE1009 dataset was downloaded from Gene Expression Omnibus database and the gene expression profile of glomeruli from diabetic nephropathy patients and those from healthy individuals were compared. The protein-protein interaction network for differentially expressed genes was constructed and enriched. In addition, topology of the network was analyzed to identify the genes with high centrality parameters and then pathway enrichment analysis was performed. We found 49 genes to be variably expressed between the two groups. The network of these genes had few interactions so it was enriched and a network with 137 nodes was constructed. Based on different parameters, 34 nodes were considered to have high centrality in this network. Pathway enrichment analysis with these central genes identified 62 inter-connected signaling pathways related to diabetic nephropathy. Interestingly, the central nodes were more informative for pathway enrichment analysis compared to all network nodes and also 49 differentially expressed genes. In conclusion, we here show that central nodes in protein interaction networks tend to be present in pathways that co-occur in a biological state. Also, this study suggests a computational method for inferring underlying mechanisms of complex disorders from raw high-throughput data.

Keywords: Diabetic nephropathy; Microarray analysis; Protein interaction maps; Systems biology

References

  1. PLoS One. 2014 Oct 22;9(10):e111347 - PubMed
  2. PLoS Comput Biol. 2008 Jun 20;4(6):e1000096 - PubMed
  3. PLoS One. 2010 Jun 14;5(6):e11095 - PubMed
  4. Nucleic Acids Res. 2009 Jan;37(Database issue):D885-90 - PubMed
  5. J Clin Invest. 2007 Mar;117(3):524-9 - PubMed
  6. Genome Res. 2003 Nov;13(11):2498-504 - PubMed
  7. PLoS Genet. 2006 Jun 2;2(6):e88 - PubMed
  8. Trends Genet. 2004 Jun;20(6):227-31 - PubMed
  9. Nat Med. 2012 Mar 11;18(4):580-8 - PubMed
  10. Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1028-33 - PubMed
  11. Exp Diabesity Res. 2003 Oct-Dec;4(4):271-85 - PubMed
  12. Bioinformatics. 2009 Apr 15;25(8):1091-3 - PubMed
  13. Adv Chronic Kidney Dis. 2010 May;17(3):265-70 - PubMed
  14. Nature. 2001 May 3;411(6833):41-2 - PubMed
  15. Gastroenterology. 2014 Jan;146(1):46-62 - PubMed
  16. Diabetes Res Clin Pract. 2008 Nov 13;82 Suppl 1:S38-41 - PubMed
  17. Kidney Int. 2004 Sep;66(3):1107-14 - PubMed
  18. Sci Signal. 2014 Feb 04;7(311):ra12 - PubMed
  19. Bioinformatics. 2013 Mar 1;29(5):661-3 - PubMed
  20. Mol Biol Evol. 2005 Apr;22(4):803-6 - PubMed
  21. J Histochem Cytochem. 2009 Jul;57(7):623-31 - PubMed
  22. Hum Genomics. 2011 Oct;5(6):538-68 - PubMed
  23. Wiley Interdiscip Rev Syst Biol Med. 2014 Jan-Feb;6(1):77-91 - PubMed
  24. Am J Kidney Dis. 2004 Apr;43(4):636-50 - PubMed
  25. PLoS One. 2009 Dec 07;4(12):e8100 - PubMed

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