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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

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

Fig. 5

Diminished angiogenic remodeling in α5-EC-KO mice during the pre-symptomatic phase of EAE. a. Frozen sections of lumbar spinal cord taken from α5-EC-KO and WT littermate control mice at the pre-symptomatic phase of EAE were stained with antibodies specific for CD31 (AlexaFluor-488) and the cell proliferation marker Ki67 (Cy-3). Scale bar = 100 μm. b and c. Quantification of endothelial cell proliferation (b) and vascular density (c) in α5-EC-KO vs. WT littermate mice in disease-free (abbreviated to D-F in panels b and c), pre-symptomatic and symptomatic EAE conditions. Results are expressed as the mean ± SEM (n = 4 mice/group). Note that WT control mice showed robust endothelial proliferation during the pre-symptomatic phase of EAE, but this response was markedly reduced in α5-EC-KO mice. At the symptomatic phase, endothelial proliferation was much lower and similar in the two strains. Furthermore, in WT mice, endothelial proliferation resulted in enhanced vessel density compared to disease-free conditions, but this increase was blunted in α5-EC-KO mice. d. High power image of CD31/Ki67 dual-IF showing multiple proliferating endothelial cells (arrows) in WT mice at the pre-symptomatic phase of EAE. Scale bar = 25 μm. * p < 0.05 vs. WT. e. Quantification of proliferation of α5 integrin null and WT brain endothelial cells (BECs). Results are expressed as the mean ± SEM of 4 separate experiments. Note that TNF-α promoted proliferation of WT BECs but α5 integrin null BECs showed reduced proliferation rates and were largely unresponsive to TNF-α. * p < 0.05

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