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Article Open Access

Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis

  • Authors:
    • Guangda Xin
    • Rui Chen
    • Xiaofei Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Nephrology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China, Department of Pediatrics, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China
    Copyright: © Xin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2651-2660
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    Published online on: July 16, 2018
       https://doi.org/10.3892/mmr.2018.9284
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Abstract

The aim of the present study was to explore the candidate genes, chemicals and mechanisms of congenital obstructive nephropathy (CON). The gene expression profiles of GSE48041, including 24 kidney tissue samples from megabladder (mgb‑/‑) mouse were downloaded from the Gene Expression Omnibus database. Samples were divided into 4 groups: Control, mild, moderate and severe. Differentially expressed genes (DEGs), protein‑protein interaction network, Kyoto Encyclopedia of Genes and Genomes pathways and transcription factor (TF)‑target gene analyses were performed on Set 1 (mild, moderate and severe groups), while Gene Ontology (GO) function enrichment analysis and chemical investigation were performed on Set 2 (severe group). A total of 187 and 139 DEGs were obtained in Set 1 and Set 2, respectively. Chemical carcinogenesis [enriched by genes such as Carbonyl reductase 1 (CBR1)] was one of the most prominent pathways in Set 1. GO analysis for Set 2 revealed that DEGs were mainly assembled in functions such as cellular response to interleukin‑1 and cellular response to tumor necrosis. Furthermore, genes such as Fos Proto‑Oncogene (FOS) were co‑regulated by TFs including RNA polymerase II subunit A (Polr2a) and serum response factor (Srf). Chemical cyclosporine served the most important role in Set 2 by targeting several DEGs in Set 2. DEGs such as CBR1 and FOS, TFs including Polr2a and Srf, and pathways such as chemical carcinogenesis may serve important roles in the process of CON. Interleukin‑1 and tumor necrosis function may be novel targets for CON gene therapy. Furthermore, cyclosporine may be a promising option for future CON therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Xin G, Chen R and Zhang X: Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis. Mol Med Rep 18: 2651-2660, 2018.
APA
Xin, G., Chen, R., & Zhang, X. (2018). Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis. Molecular Medicine Reports, 18, 2651-2660. https://doi.org/10.3892/mmr.2018.9284
MLA
Xin, G., Chen, R., Zhang, X."Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis". Molecular Medicine Reports 18.3 (2018): 2651-2660.
Chicago
Xin, G., Chen, R., Zhang, X."Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis". Molecular Medicine Reports 18, no. 3 (2018): 2651-2660. https://doi.org/10.3892/mmr.2018.9284
Copy and paste a formatted citation
x
Spandidos Publications style
Xin G, Chen R and Zhang X: Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis. Mol Med Rep 18: 2651-2660, 2018.
APA
Xin, G., Chen, R., & Zhang, X. (2018). Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis. Molecular Medicine Reports, 18, 2651-2660. https://doi.org/10.3892/mmr.2018.9284
MLA
Xin, G., Chen, R., Zhang, X."Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis". Molecular Medicine Reports 18.3 (2018): 2651-2660.
Chicago
Xin, G., Chen, R., Zhang, X."Candidate gene and mechanism investigations in congenital obstructive nephropathy based on bioinformatics analysis". Molecular Medicine Reports 18, no. 3 (2018): 2651-2660. https://doi.org/10.3892/mmr.2018.9284
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