Fig. 6

CMH specifically upregulates the laminin isoform-111 in the parenchymal layer of the vascular basement membrane. Frozen sections of lumbar spinal cord taken from EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD45 (AlexaFluor-488) and the laminin α1 subunit (Cy-3) in panel A, CD31 (AlexaFluor-488) and the laminin α2 subunit (Cy-3) in panel C, or type IV collagen (Cy-3) and laminin (AlexaFluor-488) in panel D. Scale bar = 100 μm. b. Quantification of vascular laminin α1 subunit expression. Results are expressed as the mean ± SEM (n = 6 mice/group). Note that CMH enhanced laminin α1 expression within the parenchymal basement membrane but had no observable effect on laminin α2 expression. Also note that collagen IV is expressed only within the endothelial layer of the vascular basement membrane and expression is not altered by CMH (d). ** p < 0.01. e. CD31/CD45/laminin α1 triple-IF staining of EAE spinal cord under normoxic or CMH conditions. Note that compared to normoxic conditions, the parenchymal vascular basement membrane in CMH-treated mice contains higher levels of laminin-111 and is more effective at restricting the transmigration of CD45+ leukocytes