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Alteration of the microRNA expression profile in familial Mediterranean fever patients

Yeliz Z Akkaya-Ulum1, Banu Balci-Peynircioglu1, Omer Karadag2

  • 1Department of Medical Biology, Hacettepe University, Ankara, Turkey.

Clinical and Experimental Rheumatology
|December 12, 2017
PubMed
Abstract

Insights

Familial Mediterranean Fever (FMF) disease shows variations potentially due to epigenetic factors. This study identified differentially expressed microRNAs (miRNAs) linked to inflammatory pathways in FMF patients, suggesting their role in disease pathogenesis.

Area of Science:

  • Genetics and Molecular Biology
  • Immunology
  • Epigenetics

Background:

  • Familial Mediterranean Fever (FMF) exhibits phenotypic heterogeneity, suggesting factors beyond simple monogenic inheritance.
  • Epigenetic modifications, particularly microRNAs (miRNAs), are hypothesized to contribute to FMF's variable disease expression.

Purpose of the Study:

  • To investigate the potential involvement of miRNAs in the pathogenesis of FMF.
  • To identify differentially expressed miRNAs in FMF patients compared to healthy controls and carriers.

Main Methods:

  • Whole blood RNA samples from healthy controls, FMF patients (homozygotes and heterozygotes), and healthy carriers were analyzed using miRNA arrays.
  • Data analysis involved Multi Experiment Viewer (MeV) for candidate miRNA identification and qRT-PCR for validation.
  • Bioinformatics tools were employed for pathway analysis of identified miRNAs.

Main Results:

  • Fourteen significant miRNAs were identified across the study groups.
  • miR-20a-5p and miR-574-3p were upregulated in FMF patients, while miR-197-3p was downregulated.
  • let-7d-3p and miR-574-3p were found to be upregulated in heterozygote patients, with associations to inflammatory pathway genes.

Conclusions:

  • Several miRNAs are differentially expressed in both homozygote and heterozygote FMF patients.
  • These miRNAs, particularly those associated with inflammatory pathways, may play a significant role in the pathogenesis and expression of FMF.

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