Research Paper Volume 15, Issue 19 pp 9913—9947

Figure 3. Impact of aging and reduced double-strand DNA break repair on arterial DNA damage, senescence, and endothelium-dependent and -independent vasodilation. (A) Representative images of immunofluorescence for the DNA damage marker 53BP1 performed in aortic segments of Old ATM +/+ and Old ATM+/− mice. Green is elastin (ELN) autofluorescence from tunica media. N = 4–6 per group. (B) Percentage of aortic cells containing one or more 53BP1 foci. (C) Aortic mRNA expression of atm and senescence-related genes. N = 5–10 per group. (D) Mesenteric artery dose-response curves to increasing doses of the endothelium-dependent vasodilator acetylcholine in the absence and presence of the nitric oxide synthase inhibitor L-NAME. N = 8–14 per group. (E) Maximal acetylcholine (ACh) vasodilation in mesenteric arteries in the absence and presence of L-NAME. N = 8–14 per group. (F) Mesenteric artery dose-response curves to increasing doses of the endothelium-independent vasodilator sodium nitroprusside. N = 14–16 per group. Individual data points with black borders denote female mice. Individual data points matching group colors denote male mice. ^*p < 0.05 vs. Old ATM +/+ Acetylcholine dose-response curve in the absence of L-NAME. ^†p < 0.05 vs. Acetylcholine dose-response curve in the absence of L-NAME from the same group. Scale bars are 50 μm.