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MiR103a-3p and miR107 are related to adaptive coping in a cluster of fibromyalgia patients

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  • Alexandra Braun
  • Dimitar Evdokimov
  • Johanna Frank
  • Claudia Sommer
  • Nurcan Üçeyler

Abstract

Background: MicroRNA (miRNA) mainly inhibit post-transcriptional gene expression of specific targets and may modulate disease severity. Objective: We aimed to identify miRNA signatures distinguishing patient clusters with fibromyalgia syndrome (FMS). Subjects and methods: We previously determined four FMS patient clusters labelled “maladaptive”, “adaptive”, “vulnerable”, and “resilient”. Here, we cluster-wise assessed relative gene expression of miR103a-3p, miR107, miR130a-3p, and miR125a-5p in white blood cell (WBC) RNA of 31 FMS patients and 16 healthy controls. Sum scores of pain-, stress-, and resilience-related questionnaires were correlated with miRNA relative gene expression. A cluster-specific speculative model of a miRNA-mediated regulatory cycle was proposed, and its potential targets verified by the online tool “target scan human”. Results: One-way ANOVA revealed lower gene expression of miR103a-3p, miR107, and miR130a-3p in FMS patients compared to controls (p

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  • Alexandra Braun & Dimitar Evdokimov & Johanna Frank & Claudia Sommer & Nurcan Üçeyler, 2020. "MiR103a-3p and miR107 are related to adaptive coping in a cluster of fibromyalgia patients," PLOS ONE, Public Library of Science, vol. 15(9), pages 1-12, September.
    • Handle: RePEc:plo:pone00:0239286
    DOI: 10.1371/journal.pone.0239286
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    1. Qiulun Lu & Zejun Ma & Ye Ding & Tatiana Bedarida & Liming Chen & Zhonglin Xie & Ping Song & Ming-Hui Zou, 2019. "Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    2. Qiulun Lu & Zejun Ma & Ye Ding & Tatiana Bedarida & Liming Chen & Zhonglin Xie & Ping Song & Ming-Hui Zou, 2019. "Publisher Correction: Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis," Nature Communications, Nature, vol. 10(1), pages 1-1, December.
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