Figure 3
Figure 3. Enlargement of blood vessels during acute skin inflammation. (A-B) Immunofluorescence analyses for the blood vessel-specific marker MECA-32 and subsequent morphometric quantification showed a significant increase in blood vessel number per millimeter basement membrane (BM) in K14-VEGF-C and K14-VEGF-D Tg mice at 2 days after oxazolone challenge (2-day oxa), compared with untreated mice (A). The blood vessel size was also increased in all 3 groups of mice at 2 days of oxazolone challenge, compared with untreated mice of the same genotype (B). There was no significant difference in blood vessel number (A,C) or blood vessel size (B,D) at 2 days after oxazolone challenge or UVB irradiation (2-day UVB) between K14-VEGF-C, K14-VEGF-D Tg, and wild-type mice. (A-B) Quantification of ear skin. (C-D) Quantification of back skin. (A-D) Data are mean ± SD. *P ≤ .05. **P ≤ .01. ***P ≤ .001. ns indicates not significant versus untreated mice of the same genotype.

Enlargement of blood vessels during acute skin inflammation. (A-B) Immunofluorescence analyses for the blood vessel-specific marker MECA-32 and subsequent morphometric quantification showed a significant increase in blood vessel number per millimeter basement membrane (BM) in K14-VEGF-C and K14-VEGF-D Tg mice at 2 days after oxazolone challenge (2-day oxa), compared with untreated mice (A). The blood vessel size was also increased in all 3 groups of mice at 2 days of oxazolone challenge, compared with untreated mice of the same genotype (B). There was no significant difference in blood vessel number (A,C) or blood vessel size (B,D) at 2 days after oxazolone challenge or UVB irradiation (2-day UVB) between K14-VEGF-C, K14-VEGF-D Tg, and wild-type mice. (A-B) Quantification of ear skin. (C-D) Quantification of back skin. (A-D) Data are mean ± SD. *P ≤ .05. **P ≤ .01. ***P ≤ .001. ns indicates not significant versus untreated mice of the same genotype.

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