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. Author manuscript; available in PMC: 2009 Aug 28.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2009 Jan 15;29(4):495–502. doi: 10.1161/ATVBAHA.108.180349

Fig.5. Both NO and ASK1 pathways contribute to ischemia-induced angiogenesis.

Fig.5

a–b. eNOS deletion had no effects on ischemia-induced ASK1 activation. WT, eNOS-KO and eNOS-KO/Trx2-TG mice were subjected to ischemia ligation, tissues were harvested on day 7. Trx2 expression was determined by Western blot with anti-Trx2. Phospho- and total ASK1 were determined by Western blot with a phospho-specific antibody. Relative ratios of p-ASK1/ASK1 are shown, with untreated WT as 1.0. c. Effects of eNOS deletion on Trx2 augmented ischemia-induced flow recovery. WT, eNOS-KO and eNOS-KO/Trx2-TG mice were subjected to ischemia ligation. blood flow was measured as described in Fig.1. Data from different mice are shown in graphics and n=4 for each strain. *, p<0.05. d. A model for Trx2 function in ischemia-mediated angiogenesis (see text for details). Our previous and current data support that Trx2 maintains EC function by two parallel pathways – scavenging ROS to increase NO bioavailability and inhibiting ASK1 activity to enhance EC survival, leading to enhanced ischemia-mediated arteriogenesis and angiogenesis.