Pediatric Rheumatology

, 11:A187 | Cite as

OR10-004 - Circulating micrornas in TRAPS

  • OM Lucherini
  • L Obici
  • M Ferracin
  • V Fulci
  • MF McDermott
  • G Merlini
  • I Muscari
  • F Magnotti
  • LJ Dickie
  • M Galeazzi
  • M Negrini
  • CT Baldari
  • R Cimaz
  • L Cantarini
Open Access
Meeting abstract
  • 371 Downloads

Keywords

Anakinra Serum miRNAs Autoinflammatory Disorder Agilent Microarrays Disease Penetrance 

Introduction

To the best of our knowledge circulating miRNAs in TRAPS, as well as in other monogenic autoinflammatory disorders have never been investigated.

Objectives

To evaluate circulating microRNAs (miRNAs) levels in patients with tumor necrosis factor-receptor associated periodic syndrome (TRAPS), in comparison to healthy controls, and to correlate their levels to parameters of disease activity and/or disease severity.

Methods

Expression levels of circulating miRNAs were measured by Agilent microarrays in 29 serum samples from 15 TRAPS patients carrying mutations known to be associated with high disease penetrance and 8 healthy controls. Differentially expressed and clinically relevant miRNAs were detected using GeneSpring GX software.

Results

We identified a 6 miRNAs signature able to discriminate TRAPS from healthy controls. Moreover, 4 miRNAs were differentially expressed between patients treated with the interleukin (IL)-1 receptor antagonist anakinra and untreated patients. Of these, miR-92a-3p expression was found to be reduced in untreated patients, while its expression levels were similar to healthy controls in samples obtained during anakinra treatment. MiR-92b levels were inversely correlated with the number of fever attacks/year during the 1st year from the index attack of TRAPS, while miR-377-5p levels were positively correlated with serum amyloid A (SAA) circulating levels.

Conclusion

Serum miRNAs levels show a baseline pattern in TRAPS, and may serve as potential markers of response to therapeutic intervention.

Notes

Copyright information

© Lucherini et al; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Authors and Affiliations

  • OM Lucherini
    • 1
  • L Obici
    • 2
  • M Ferracin
    • 3
  • V Fulci
    • 4
  • MF McDermott
    • 5
  • G Merlini
    • 6
  • I Muscari
    • 7
  • F Magnotti
    • 1
  • LJ Dickie
    • 5
  • M Galeazzi
    • 7
  • M Negrini
    • 3
  • CT Baldari
    • 8
  • R Cimaz
    • 9
  • L Cantarini
    • 10
  1. 1.Department of Medical Sciences, Surgical and Neuroscience. Rheumatology UnitUniversità di SienaSienaItaly
  2. 2.Amyloid Research and Treatment Center, Fondazione IRCCS Policlinico San Matteo, and Department of Molecular MedicineUniversity of PaviaPaviaItaly
  3. 3.Laboratory for Technologies of Advanced Therapies (LTTA) and Department of Morphology, Surgery and Experimental MedicineUniversity of FerraraFerraraItaly
  4. 4.Dipartimento di Biotecnologie Cellulari ed Ematologia, Sezione di Genetica Molecolare, SapienzaUniversità di RomaRomaItaly
  5. 5.NIHR-Leeds Musculoskeletal Biomedical Research Unit (NIHR-LMBRU)Leeds Institute of Rheumatic and Musculoskeletal MedicineLeedsUK
  6. 6.University of PaviaPaviaItaly
  7. 7.Università di SienaSienaItaly
  8. 8.Department of Life SciencesUniversità di SienaSienaItaly
  9. 9.Department of Pediatrics, Rheumatology UnitAnna Meyer Children's Hospital and University of FlorenceFlorenceItaly
  10. 10.Department of Medical Sciences, Surgical and Neuroscience. Rheumatology UnitUniversity of SienaSienaItaly

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