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. 2024 Aug 31;21:214. doi: 10.1186/s12974-024-03206-4

Fig. 2.

Fig. 2

LILRB4 exhibits high expression in microglia during tMCAO in mice. (A) Overview of experimental design. (B) Representative laser speckle rheogram from WT tMCAO mice, IR: Ischaemia-Reperfusion. (C) Representative images of TTC staining of brain sections from tMCAO mice. (D, E) Increased expression of LILRB4 in stroke mice brains compared to controls, showing an increasing trend from day 1 to day 3. (n = 6; **p = 0.0082, ***p = 0.0090). (F) qPCR analysis of LILRB4 expression after tMCAO 1 h. (n = 6; ***p = 0.0003, **p = 0.0093). (G, H) FACS analysis of LILRB4 expression in microglia after tMCAO. (n = 6; ***p = 0.0008, **p = 0.0073). (I) Specimen sites of Immunofluorescent staining. (J) Representative photograph of Immunofluorescent staining at low magnification field of view. Scale bars, 100 μm. (K, L) Immunofluorescence staining showing increased LILRB4 expression at 1 and 3 days post-infarction. Scale bars, 50 μm. (n = 6; ****p<0.0001, **p = 0.0026). (M) LILRB4 and GFAP/NeuN/Iba − 1 immunofluorescence double staining, confirming LILRB4 localization in Iba-1+ microglia. Scale bar, 50/20µm. (N) Colocalization analysis of IBA-1 and LILRB4 in (M). ImageJ quantification