• Pain Med · Oct 2016

    Correlation Between DNA Methylation of TRPA1 and Chronic Pain States in Human Whole Blood Cells.

    • Norihiko Sukenaga, Yasuko Ikeda-Miyagawa, Daisuke Tanada, Takashi Tunetoh, Susumu Nakano, Takae Inui, Kazumi Satoh, Hiroai Okutani, Koichi Noguchi, and Munetaka Hirose.
    • *Department of Anesthesiology and Pain Medicine.
    • Pain Med. 2016 Oct 1; 17 (10): 1906-1910.

    ObjectivesNeuro-immune interactions with functional changes in the peripheral blood cells including changes in the transient receptor potential ankyrin 1 (TRPA1) appear to play a pivotal role in the development of chronic pain in humans. The aim of this study was to examine the association between TRPA1 DNA methylation in whole blood cells and the pain states in chronic pain patients.MethodsAfter collecting blood samples from 12 chronic pain patients, the authors measured DNA methylation levels in whole blood cells. Significant associations between the patient's demographic data and the chronic pain states were determined by a multiple linear regression analysis that used age, body mass index, pain duration, depression, anxiety, cognitive impairment, activities of daily living, neuropathic pain, and pain states as the dependent variables, and the TRPA1 DNA methylation levels as the independent variables.ResultsMultiple regression analysis revealed a significant correlation between increases of the methylation levels of the CpG island in the TRPA1 gene and increases in the number of neuropathic pain symptoms, which were evaluated using the Douleur Neuropathique 4 (DN4) questionnaire. Decreases in the TRPA1 mRNA expression were also significantly related to increases in the DN4 score. The presence of a burning sensation, which is one of pain symptoms in the DN4 questionnaire, was significantly correlated with the increase in DNA methylation level of TRPA1.ConclusionsTRPA1 DNA methylation levels in whole blood cells appear to be associated with pain symptoms in chronic pain patients.© 2016 American Academy of Pain Medicine. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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