Fig. 3.
Fig. 3. Increased angiogenesis and inflammation in cutaneous DTH reactions elicited in TSP-2–deficient mice. / No apparent morphologic differences were found between the untreated ear skin of wild-type (A) and TSP-2–deficient mice (B). However, CD31 stains revealed increased skin vascularization in TSP-2–deficient mice (D), as compared with wild-type mice (C). Highly increased edema formation and inflammatory infiltration in the skin of TSP-2–deficient mice (F) at 24 hours after antigen challenge, as compared with wild-type mice (E). CD31 stains demonstrated enhanced angiogenesis 24 hours after challenge in TSP-2–deficient mice (H), as compared with wild-type mice (G). Twenty-eight days after challenge, the ear thickness of wild-type mice (I) and TSP-2–deficient mice (J) returned to normal levels, whereas blood vessels in the skin of TSP-2–deficient mice remained enlarged (J). Hematoxylin/eosin stains were used to produce panels A, B, E, and F, and CD31 stains for panels C, D, and G-J. Scale bars = 125 μm.

Increased angiogenesis and inflammation in cutaneous DTH reactions elicited in TSP-2–deficient mice.

No apparent morphologic differences were found between the untreated ear skin of wild-type (A) and TSP-2–deficient mice (B). However, CD31 stains revealed increased skin vascularization in TSP-2–deficient mice (D), as compared with wild-type mice (C). Highly increased edema formation and inflammatory infiltration in the skin of TSP-2–deficient mice (F) at 24 hours after antigen challenge, as compared with wild-type mice (E). CD31 stains demonstrated enhanced angiogenesis 24 hours after challenge in TSP-2–deficient mice (H), as compared with wild-type mice (G). Twenty-eight days after challenge, the ear thickness of wild-type mice (I) and TSP-2–deficient mice (J) returned to normal levels, whereas blood vessels in the skin of TSP-2–deficient mice remained enlarged (J). Hematoxylin/eosin stains were used to produce panels A, B, E, and F, and CD31 stains for panels C, D, and G-J. Scale bars = 125 μm.

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