Thromboxane A2/Prostaglandin H2 Receptor Activation Mediates Angiotensin II–Induced Postischemic Neovascularization
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Figure 1. A, Quantitative evaluation of TXB2 content in plasma. Quantitative evaluation of microangiography (B) and foot perfusion (C) 21 days after femoral artery occlusion. Values are mean±SEM (n=7). **P<0.01 vs sham-operated nonischemic mice. ††P<0.01 vs control ischemic mice. Sham indicates untreated sham-operated mice without hindlimb ischemia; Isch+ no treatment, untreated mice with hindlimb ischemia; Isch + S18886(5), mice with hindlimb ischemia treated with S18886 at 5 mg/kg per day; Isch + S18886(10), mice with hindlimb ischemia treated with S18886 at 10 mg/kg per day; Isch + Ram(10), mice with hindlimb ischemia treated with ramatroban at 10 mg/kg per day; and Isch + Asp, mice with hindlimb ischemia treated with aspirin at 30 mg/kg per day.
Figure 2. Quantitative evaluation of microangiography (A), capillary density (B, capillary appears in white, arrows indicating representative examples of fibronectin-positive capillaries), and paw perfusion (C) 21 days after femoral artery occlusion. Values are mean±SEM. n=7 per group. *P<0.05 vs control ischemic mice. †P<0.05 vs Ang II-treated (0.3 mg/kg per day) ischemic mice. Cont indicates untreated mice with hindlimb ischemia; Ang II, mice with hindlimb ischemia treated with Ang II; Ang II + S 18886, mice with hindlimb ischemia treated with Ang II and S18886 at 10 mg/kg per day; Ang II + Ram, mice with hindlimb ischemia treated with Ang II and ramatroban at 10 mg/kg per day; Ang II + Asp, mice with hindlimb ischemia treated with Ang II and aspirin (30 mg/kg per day); Ang II + Cand, mice with hindlimb ischemia treated with Ang II and the AT1 receptor blocker candesartan (20 mg/kg per day); Isch, ischemic leg; N.Isch, nonischemic legs.
Figure 3. A, Representative photomicrograph and quantitative evaluation of Mac-3–positive cells in ischemic tissue. B, Representative Western blot and quantitative evaluation of VEGF-A protein content. As a protein loading control, membranes were stripped, incubated with a goat polyclonal antibody directed against total actin. Values are mean±SEM, n=5 per group. *P<0.05 vs control ischemic mice. †P<0.05 vs Ang II-treated ischemic mice. Cont indicates untreated mice with hindlimb ischemia; Ang II, mice with hindlimb ischemia treated with Ang II; Ang II + S 18886, mice with hindlimb ischemia treated with Ang II and S18886 at 10 mg/kg per day; Ang II + Ram, mice with hindlimb ischemia treated with Ang II and ramatroban at 10 mg/kg per day; Ang II + Asp, mice with hindlimb ischemia treated with Ang II and aspirin (30 mg/kg per day); Ang II + Cand, mice with hindlimb ischemia treated with Ang II and the AT1 receptor blocker candesartan (20 mg/kg per day); Isch, ischemic leg.
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- Thromboxane A2/Prostaglandin H2 Receptor Activation Mediates Angiotensin II–Induced Postischemic NeovascularizationFrédéric Michel, Jean-Sébastien Silvestre, Ludovic Waeckel, Stefano Corda, Tony Verbeuren, Jean Paul Vilaine, Michel Clergue, Micheline Duriez and Bernard I. LevyArteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:488-493, originally published February 16, 2006https://doi.org/10.1161/01.ATV.0000201969.93348.74
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- Thromboxane A2/Prostaglandin H2 Receptor Activation Mediates Angiotensin II–Induced Postischemic NeovascularizationFrédéric Michel, Jean-Sébastien Silvestre, Ludovic Waeckel, Stefano Corda, Tony Verbeuren, Jean Paul Vilaine, Michel Clergue, Micheline Duriez and Bernard I. LevyArteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:488-493, originally published February 16, 2006https://doi.org/10.1161/01.ATV.0000201969.93348.74