Fig. 3
From: Endothelial -targeted CD39 is protective in a mouse model of global forebrain ischaemia
Gene expression of A2B receptors were significantly changed after anti-VCAM-CD39 treatment, and antagonism of the adenosine receptors removed the protective effect of anti-VCAM-CD39 in vitro, confirming that the protective mechanism of anti-VCAM-CD39 is through the generation of adenosine. Expression of (A) A2B receptor expression was found to be significantly upregulated after treatment with anti-VCAM-CD39. (Data is Mean ± SEM; Saline: n = 6–15, anti-VCAM-CD39: n = 6–13; *p < 0.05, **p < 0.01; Unpaired t-test). (B) Systemic Adenosine and ATP concentration (expressed as a ratio) in plasma was found to be significantly increased after anti-VCAM-CD39 treatment (Data is Mean ± SEM; Saline: n = 14, anti-VCAM-CD39: n = 13; *p < 0.05; Unpaired t-test). (C) Analysis of LDH levels In Vitro post-OGD determined that anti-VCAM-CD39 was able to significantly reduce necrotic cell death, but with co-treatment of CGS-15,943, this protective effect ceases (Data is Mean ± SEM; Saline: n = 13, anti-VCAM-CD39: n = 13; CGS-treated: n = 5; **p < 0.01, ***p < 0.001; Mixed-effects analysis)