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. Author manuscript; available in PMC: 2016 Apr 10.
Published in final edited form as: Circ Res. 2015 Feb 26;116(8):1336–1345. doi: 10.1161/CIRCRESAHA.116.304881

Figure 7. CypD knockdown accelerates wound healing and neovascularization in vivo.

Figure 7

(A) Wound area progression in WT and CypD KO mice after skin excision of mouse pinnae with a biopsy punch. Measurements were normalized to the day 1 wound size (mean ± SEM, n=6/group). (B) Representative OMAG images of microvascular changes during wound healing in WT and CypD KO mice, at days 1 and 14 after wounding (structure images of pinna cross-section overlaid with 3D view of OMAG vasculature, red, and projection view images of OMAG vasculature, yellow). (C) Vessel area density in WT and CypD KO mice at baseline and wound location at 14 days post wounding calculated from projection OMAG images (mean ± SEM, n=3 mice/group). (D) Genetic or pharmacological inhibition of mPTP in ECs increases matrix Ca2+ and stimulates NADH accumulation. Simultaneously a decrease in cytosolic NAD+/NADH ratio downregulates SIRT1 and PTEN resulting in Akt activation and increased angiogenesis. NMN supplementation restores NAD+/NADH ratio and recovers the phenotype.