Supplementary Materials

Supplementary Materials for:

MEG3-4 is a miRNA decoy that regulates IL-1β abundance to initiate and then limit inflammation to prevent sepsis during lung infection

Rongpeng Li, Lizhu Fang, Qinqin Pu, Huimin Bu, Pengcheng Zhu, Zihan Chen, Min Yu, Xuefeng Li, Timothy Weiland, Arvind Bansal, Shui Qing Ye, Yuquan Wei, Jianxin Jiang,* Min Wu*

*Corresponding author. Email: min.wu{at}med.und.edu (M.W.); hellojjx{at}126.com (J.J.)

This PDF file includes:

  • Fig. S1. Characterization of lncRNA MEG3.
  • Fig. S2. MEG3-4 inhibition signaling in alveolar macrophage cells is TLR4-specific during S. aureus infection.
  • Fig. S3. Immunoblotting validation of signaling factors in inhibitor- or activator-treated MH-S cells.
  • Fig. S4. Dissection of signaling molecules in PAO1-infected MH-S cells.
  • Fig. S5. Densitometric quantification of the immunoblotting data.
  • Fig. S6. Restoration of the phenotype in a MEG3-4–overexpressing model.
  • Fig. S7. Imaging of pyroptosis in MH-S cells.
  • Fig. S8. Functional analysis of miRNAs generated by MEG3-4.
  • Fig. S9. miR-138 regulates IL-1β expression and cell viability in alveolar macrophages.
  • Fig. S10. miR-138 enhances host defense against P. aeruginosa by repressing IL-1β expression in mouse lungs.
  • Fig. S11. MEG3-4 overexpression phenotypes in mice were reversed by treatment with 138-m.
  • Fig. S12. Analysis of MEG3 function and expression in human alveolar macrophages.
  • Fig. S13. MEG3-4 overexpression inhibits p53 expression in mouse B16 melanoma tumor cells.
  • Table S1. lncRNA expression in response to PAO1 infection.
  • Table S2. Primers used in this study.

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