Fig. 6

Pharmacological blockade of TNFR1, but not TNFR2, reduced vascular expression of β3 integrin in the cerebral ischemic penumbra. Frozen sections of ischemic penumbra taken from mice after 4, 7, or 14 days reperfusion following 90 min MCAO and having received daily i.c.v. injections of antibodies against TNFR1 or TNFR2 or control IgG, were dual-stained with antibodies against CD31 (AlexaFluor-488) and β3 integrin (Cy-3). a After 4 days reperfusion following MCAO, vascular expression of the β3 integrin in the ischemic penumbra of mice receiving the TNFR1 but not TNFR2 antibody (at dose of 50 ng/day) was significantly lower than control mice. Scale bar = 100 μm. b Quantification of β3 integrin-positive vessels, in which each experiment was performed with five different animals at different time-points post-ischemia. Results are expressed as the mean ± SEM of the number of β3 integrin-positive vessels per FOV. Note that the anti-TNFR1 antibody (at doses of 50 and 100 ng/day), but not the anti-TNFR2 antibody, significantly reduced endothelial expression of β3 integrin in the ischemic penumbra at 4 and 7 days post-ischemia. *P < 0.05 versus control