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. 2020 Mar 24;94(12):e1281–e1293. doi: 10.1212/WNL.0000000000008868

Figure 5. Soluble vascular endothelial (sVE)-cadherin-induced activation of microglia is mediated by a MyD88 signaling pathway.

Figure 5

(A) Scheme of experimental design of in vitro cultured microglia cotreated with sVE-cadherin and MyD88-inhibitor peptide. Immunofluorescence was performed to evaluate NFκB translocation, cell soma size, and reactive oxygen species (ROS). Western blots were performed to measure the expression of inducible nitric oxide synthase (iNOS) and interleukin (IL)-1β. (B) Nuclear translocation of NFκB (after 1 hour incubation of microglia with sVE-cadherin) is decreased by cotreatment with an inhibitor to MyD88 (p = 0.022 with Wilcoxon signed-rank test, n = 4). (C) Cotreatment with an inhibitor to MyD88 decreases sV-cadherin-induced increase inmicroglial metabolism/viability. WST (C.a.): p = 0.029 in Mann-Whitney U test (n = 4); lactate dehydrogenase (LDH) (C.b.): p = 0.008 with Mann-Whitney U test (n = 5). (D) Cotreatment with an inhibitor to MyD88 decreases sVE-cadherin-induced increase in microglia cell size. (E) Immunostaining shows that cotreatment with an inhibitor to MyD88 decreases sVE-cadherin-induced ROS in cultured microglia (n = 2). (F, G) Cotreatment with an inhibitor to MyD88 decreases sVE-cadherin-induced microglial iNOS (F,G) andmature IL-1β expression (G): p = 0.029 (iNOS), p = 0.63 (IL-1β full-length), p = 0.029 (IL-1β mature), with Mann-Whitney U test (n = 4). Abbreviation: ROS = reactive oxygen species.