O., Gidlöf R., Sathanoori M., Magistri M.A., Faghihi C., Wahlestedt B., Olde D., Erlinge Supplementary Material for: Extracellular Uridine Triphosphate and Adenosine Triphosphate Attenuate Endothelial Inflammation through miR-22-Mediated ICAM-1 Inhibition Adenosine and uridine triphosphate (ATP and UTP) can act as extracellular signalling molecules, playing important roles in vascular biology and disease. ATP and UTP acting via the P2Y<sub>2</sub>-receptor have, for example, been shown to regulate endothelial dilatation, inflammation and angiogenesis. MicroRNAs (miRNAs), a class of regulatory, short, non-coding RNAs, have been shown to be important regulators of these biological processes. In this study, we used RNA deep-sequencing to explore changes in miRNA expression in the human microvascular endothelial cell line HMEC-1 upon UTP treatment. The expression of miR-22, which we have previously shown to target ICAM-1 mRNA in HMEC-1, increased significantly after stimulation. Up-regulation of miR-22 and down-regulation of cell surface ICAM-1 were confirmed with qRT-PCR and flow cytometry, respectively. siRNA-mediated knockdown of the P2Y<sub>2</sub>-receptor abolished the effect of UTP on miR-22 transcription. Leukocyte adhesion was significantly inhibited in HMEC-1 following miR-22 overexpression and treatment with UTP/ATP. In conclusion, extracellular UTP and ATP can attenuate ICAM-1 expression and leukocyte adhesion in endothelial cells through miR-22. MicroRNA;ICAM-1;Leukocyte adhesion;Adenosine triphosphate;Uridine triphosphate;P2Y2-receptor;miR-22 promoter;Endothelial inflammation;Extracellular nucleotides 2015-06-13
    https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Extracellular_Uridine_Triphosphate_and_Adenosine_Triphosphate_Attenuate_Endothelial_Inflammation_through_miR-22-Mediated_ICAM-1_Inhibition/5128225
10.6084/m9.figshare.5128225.v1