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. 2015 Apr 22;138(6):1598–1612. doi: 10.1093/brain/awv092

Figure 4.

Figure 4

Netrin 1 counteracts the detrimental outcome induced by inflammation on the human and murine blood–brain barrier. Production of IL8, MCP-1, IP-10, and IL6 by primary cultures of human brain-derived endothelial cells activated with 100 U/ml of TNF/IFNγ (T/I) alone or in combination with netrin 1 (N1) was measured by ELISA (A). Expression of cell adhesion molecules (ICAM1, MCAM and ALCAM) by human brain-derived endothelial cells was also determined under the same conditions using flow cytometry (B). The expression of JAM-A (C), occludin (D) and claudin-5 (E) by human brain-derived endothelial cells was measured by western blot under the same conditions. (F) Impedance readout at 1000 Hz from primary cultures of mouse brain endothelial cells exposed to IFNγ and TNF when confluent. Netrin 1 treatment was applied 30 h post-inflammation. (G) High power view of the impedance change induced by netrin 1 treatment on inflamed mouse brain endothelial cells. Data (C–E) represent the mean percentile change ± SEM of expression normalized to actin from n = 5 independent experiments. Individual points (A) represent absolute concentrations of cytokines for n = 3–10 independent experiments. (*P ≤ 0.05; **P ≤ 0.01).