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. 2001 Feb 27;98(5):2604–2609. doi: 10.1073/pnas.041359198

Figure 1.

Figure 1

Angiogenesis in collagen gels. Angiogenesis in control collagen gels (A) and VEGF (3 μg/ml) containing gels (B) in mouse cranial window was monitored for 14 days. Angiogenesis was quantified as the percentage of squares in the top nylon mesh containing at least one vessel. (A) In the control gels, eNOS−/−Rag-1−/− mice (□ KO, n = 10) showed significantly reduced angiogenesis compared with WT Rag-1−/− (○, n = 10) mice. l-NIL (an iNOS selective inhibitor)-treated Rag-1−/− mice (▵ WT/l-NIL, n = 4) showed slightly slower angiogenesis than WT/control but the difference was not significant at any time point. (B) In the VEGF gel, l-NIL treatment (▴ WT/l-NIL, n = 8) modestly reduced angiogenesis (P < 0.05 compared with nontreated Rag-1−/− mice at day 6 and day 8). Angiogenesis in eNOS−/−Rag-1−/− mice (■ KO, n = 15) was significantly reduced compared with Rag-1−/− mice (● WT, n = 16). l-NIL treatment of eNOS−/−Rag-1−/− mice (⧫ KO/l-NIL, n = 6) further delayed angiogenesis. (C) The rate of angiogenesis was calculated from time required to fill 50% of squares in the mesh, which is derived from individual angiogenic response curves (A and B). VEGF (3 ng/μl) significantly accelerated angiogenesis in Rag-1−/− (WT) mice with or without l-NIL treatment, but not in eNOS−/−Rag-1−/− (KO) mice. In both control gel and VEGF gel, l-NIL treatment slightly slowed the angiogenesis and KO showed significantly slower angiogenesis than WT mice. Inhibition of both eNOS and iNOS (KO/l-NIL) resulted in further delays in angiogenesis. *, P < 0.05 as compared with WT mice. #, P < 0.05 as compared with WT mice with l-NIL treatment.