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. 2020 May 5;117(20):11126–11135. doi: 10.1073/pnas.1920935117

Fig. 2.

Fig. 2.

CMH treatment of preexisting EAE promotes beneficial changes in vascular integrity. (A and B) Frozen sections of lumbar spinal cord taken from disease-free, EAE–normoxia or EAE–CMH mice at the peak and remission phases of disease (14 and 21 d postimmunization, respectively) were stained for CD31 (AlexaFluor-488) and fibrinogen (Cy-3) in A (scale bar, 500 μm) or CD31 (AlexaFluor-488) and VCAM-1 (Cy-3) in B (scale bar, 50 μm). (C and D) Quantification of fibrinogen leakage, expressed as the mean ± SEM percent area (C) and VCAM-1 expression, expressed as the mean ± SEM number of VCAM-1+ vessels/FOV (D). n = 6 mice per group. Note that following peak disease, CMH markedly suppressed fibrinogen leakage and endothelial expression of VCAM-1. *P < 0.05, **P < 0.01.