Fig. 1From: MLKL regulates Cx43 ubiquitinational degradation and mediates neuronal necroptosis in ipsilateral thalamus after focal cortical infarctionMLKL and Cx43 were upregulated in the ipsilateral VPN after dMCAO. (A, B) Representative microphotographs of the immunofluorescence assay of MLKL (green), NeuN/CD68/GFAP (red), and DAPI (blue) in VPN of Sham-operated group and 2w after dMCAO group, respectively (scale: 50 μm). (C, D) Representative microphotographs of the immunofluorescence assay of Cx43 and NeuN/MLKL in VPN of Sham-operated group and 2w after dMCAO group, respectively (scale: 50 μm). (E) Co-localization analysis of MLKL and NeuN, CD68 or GFAP. The histogram presents the quantitative analyses of co-staining of MLKL and NeuN, CD68, or GFAP (n = 6 in each group). (F) Representative immunoblots of MLKL and Cx43 expression, respectively, in VPN after dMCAO. The histogram presents the quantitative analyses of MLKL and Cx43 protein levels (n = 3 in each group). (G, H) Representative immunoblots of MLKL and pMLKL multimers expression, respectively, in VPN after dMCAO. (I, J) Co-immunoprecipitation analysis of MLKL and Cx43. Each bar represents mean ± standard deviation. *P < 0.05 vs. Sham-operated group and #P < 0.05 vs. contralateral to the lesion after dMCAO. dMCAO, distal middle cerebral artery occlusion model; MLKL, mixed lineage kinase domain-like protein; NeuN, neural nuclear antigen; GFAP, glial fibrillary acidic protein; CD68, cluster of differentiation 68; DAPI, 4′, 6-diamidine-2-phenylindole. Cx43, connexin 43; GAPDH, glyceraldehyde 3-phosphate dehydrogenaseBack to article page