Absence of endothelial α5β1 integrin triggers early onset of experimental autoimmune encephalomyelitis due to reduced vascular remodeling and compromised vascular integrity

Upregulated expression of fibronectin and α5 integrin on blood vessels in the lumbar spinal cord during EAE. a. Time-course of increasing EAE severity following immunization. Points represent the mean？±？SD (n？=？10 mice). b and c. Quantification of fibronectin (b) or α5 integrin (c) fluorescent signal at different time-points of EAE progression. Results are expressed as the mean？±？SEM (n？=？4 mice/group). d and e. Representative examples of fibronectin and α5 integrin staining. Dual-IF was performed on frozen sections of lumbar spinal cord taken from mice that were disease-free (D-F), or in the pre-symptomatic (Pre-sym) or peak symptomatic (Symp) phase of EAE using antibodies specific for CD31 (AlexaFluor-488) and fibronectin (Fn) (Cy-3) in panel d or for CD31 (AlexaFluor-488) and α5 integrin (Cy-3) in panel e. Scale bar？=？100？μm. Note that in the pre-symptomatic phase of EAE, vascular expression of both fibronectin and α5 integrin was significantly increased, and this enhanced expression level was maintained during the symptomatic phase of disease. * p？<？0.05 vs. disease-free contro