Supplemental Data MicroRNA-132 Potentiates Cholinergic Anti-Inflammatory Signaling by Targeting Acetylcholinesterase

To assess the involvement of miRs in the inflammatory reflex, we used FVB/N mice as well as murine RAW 264.7 macrophage-derived cells which are known to respond to LPS by production of proinflammatory mediators such as Nitric Oxide (NO) and cytokines such as IL1β, IL6, and IL-12; primary human macrophages obtained from healthy donors, which can mimic more closely the reaction of nontumor cells to the tested signals; and primary mouse peritoneal and bone marrow macrophages obtained from transgenic mice over-expressing human AChE-R devoid of the 3'UTR which contains the miR 132, 182* binding sites and presents intensified pro-inflammatory reactions (TgR) (Gilboa-Geffen et al., 2007; Pick et al., 2006; Shaked and Soreq, 2006) compared to strain-matched FVB/N controls.