Supplementary Materials

Supplementary Material for:

Up-regulation of miR-31 in human atrial fibrillation begets the arrhythmia by depleting dystrophin and neuronal nitric oxide synthase

Svetlana N. Reilly,* Xing Liu, Ricardo Carnicer, Alice Recalde, Anna Muszkiewicz, Raja Jayaram, Maria Cristina Carena, Rohan Wijesurendra, Matilde Stefanini, Nicoletta C. Surdo, Oliver Lomas, Chandana Ratnatunga, Rana Sayeed, George Krasopoulos, Timothy Rajakumar, Alfonso Bueno-Orovio, Sander Verheule, Tudor A. Fulga, Blanca Rodriguez, Ulrich Schotten, Barbara Casadei*

*Corresponding author. Email: barbara.casadei{at} (B.C.); svetlana.reilly{at}

Published 25 May 2016, Sci. Transl. Med. 8, 340ra74 (2016)
DOI: 10.1126/scitranslmed.aac4296

This PDF file includes:

  • Methods
  • Fig. S1. NOS isoforms in human and goat atrial tissue.
  • Fig. S2. nNOS knockdown or pharmacological inhibition in human atrial myocytes.
  • Fig. S3. Atrial content of dystrophin and dystrophin-associated proteins in SR and AF.
  • Fig. S4. Reporter assay with dystrophin and nNOS sensors.
  • Fig. S5. miR-31 in Ago2 immunoprecipitates and the effect of miR-31 overexpression on dystrophin mRNA decay.
  • Table S1. Clinical and demographic characteristics of patients in SR and those with persistent AF.
  • Table S2. Action potential characteristics of human and murine right atrial myocytes in the presence or absence of nNOS inhibition.
  • Table S3. In vivo cardiac electrophysiological parameters of wild-type and nNos−/− mice.
  • Table S4. Clinical and demographic characteristics of patients in SR and those with paroxysmal AF.
  • Table S5. Clinical and demographic characteristics of patients in SR before and after surgery and of those who developed postoperative AF.
  • Table S6. Predicted conserved (site 1) and poorly conserved (sites 2, 3, 4, and 5) miR-31 binding sites on the human nNOS 3′UTR.
  • Table S7. Sequences of the miR-31-5p mimic, miR-31-5p hairpin inhibitor (α-miR-31), TSBs, and negative controls for the binding sites of miR-31 on human dystrophin or nNOS (site 5) 3′UTR.

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