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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

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

Fig. 1

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 control

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