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. 2022 Sep 21;84:104275. doi: 10.1016/j.ebiom.2022.104275

Figure 3.

Figure 3

Cav-1 deficiency aggravates post-stroke microvascular inflammation and immune cell recruitment 24 h after tMCAO. (a, b) Representative immunofluorescent images showing the expression of microvascular ICAM-1 and VCAM-1 in the peri-infarct area of tMCAO mice of two genotypes 24 h after tMCAO [quantified in (c, d); n = 6 in each group; mean ± S.D; **P < 0.01 vs. WT tMCAO mice by unpaired t-test]. (e–i) Immunoblotting and quantification showing the expression of ICAM-1, VCAM-1, TNF-α, and IL-1β in brain microvessels from the peri-infarct region 24 h after surgery (a pool of 2 mice per sample, n = 5 samples in each group; mean ± S.D; **P < 0.01 vs. WT tMCAO mice by unpaired t-test). (j, k) Representative immunofluorescent images and quantification showing the Ly6G+ cells adhering to CD31+ vessels and migrated into the parenchyma at the peri-infarct area 24 h after tMCAO (n = 6 in each group; mean ± S.D; **P < 0.01 vs. WT tMCAO mice by unpaired t-test). (l, m) Representative flow cytometry graphs showing myeloid cell infiltration in the ischemic hemisphere of WT tMCAO and Cav-1-/− tMCAO mice. High expression of CD45 and CD11b (upper right quadrant), indicative of myeloid cells, were further subdivided into Ly6G-positive neutrophils and Ly6C-positive monocytes [quantified in (n–p); n = 5 in each group; mean ± S.D; *P < 0.05 vs. WT tMCAO mice by unpaired t-test)]. Scale bar: 20 μm.