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Journal of Diabetes Research
Volume 2017 (2017), Article ID 8103904, 11 pages
https://doi.org/10.1155/2017/8103904
Research Article

Gene Expression Profiling Identifies Downregulation of the Neurotrophin-MAPK Signaling Pathway in Female Diabetic Peripheral Neuropathy Patients

1Zhejiang Key Laboratory of Pathophysiology, Medical School of Ningbo University, Ningbo 315211, China
2Laboratory of Behavioral Neuroscience, Ningbo Addiction Research and Treatment Center, Medical School of Ningbo University, Ningbo 315211, China
3Department of Preventive Medicine, Medical School of Ningbo University, Ningbo 315211, China
4Department of Research and Teaching, Ningbo No. 2 Hospital, Ningbo 315010, China
5Department of Biochemistry, Medical School of Ningbo University, Ningbo 315211, China

Correspondence should be addressed to Jin Xu; nc.ude.ubn@1nijux and Lin-Dan Ji; nc.ude.ubn@nadnilij

Received 14 April 2017; Revised 14 June 2017; Accepted 2 July 2017; Published 16 August 2017

Academic Editor: Joseph F. Ndisang

Copyright © 2017 Lin Luo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus (DM). It is not diagnosed or managed properly in the majority of patients because its pathogenesis remains controversial. In this study, human whole genome microarrays identified 2898 and 4493 differentially expressed genes (DEGs) in DM and DPN patients, respectively. A further KEGG pathway analysis indicated that DPN and DM share four pathways, including apoptosis, B cell receptor signaling pathway, endocytosis, and Toll-like receptor signaling pathway. The DEGs identified through comparison of DPN and DM were significantly enriched in MAPK signaling pathway, NOD-like receptor signaling pathway, and neurotrophin signaling pathway, while the “neurotrophin-MAPK signaling pathway” was notably downregulated. Seven DEGs from the neurotrophin-MAPK signaling pathway were validated in additional 78 samples, and the results confirmed the initial microarray findings. These findings demonstrated that downregulation of the neurotrophin-MAPK signaling pathway may be the major mechanism of DPN pathogenesis, thus providing a potential approach for DPN treatment.