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Table SI. Primers used for qRT-PCR.

Figure S1. TNF-α induces miR-146a and miR-146b expression.

Figure S2. Over-expression of miR-146a inhibits monocyte adhesion to IL-1β-treated bovine aortic endothelial cells (BAEC).

Figure S3. miR-146a does not directly regulate EGR-3.

Figure S4. A potential miR-146 binding site in HuR is highly conserved across species.

Figure S5. miR-146 controls the expression of HuR mRNA.

Figure S6. HuR knock-down represses THP-1 adhesion to TNF-α-treated endothelial cells.

Figure S7. Predicted AU-rich elements (AREs) in the 3′ UTRs of genes involved in endothelial activation.

Figure S8. HuR binds to VCAM-1 and MCP-1 mRNA but does not regulate the induction of these genes by IL-1β.

Figure S9. The miR-146 targets, HuR and TRAF6, have divergent effects on the induction of inflammatory genes.

Figure S10. MicroRNAs previously implicated in regulating inflammation are not appreciably altered in miR-146a−/− mice.

Figure S11. Expression of eNOS is modestly decreased in miR-146a−/− mice.

Figure S12. KLF2 mRNA is bound by HuR and knock-down of HuR leads to increased levels of KLF2 transcripts.

Figure S13. Schematic of a miR-146 feedback loop that controls endothelial activation.

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