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It is generally accepted that angiogenesis is delayed in aging. To define the effects of age on the neovascular response, polyvinyl alcohol sponges were implanted SC in young (6–8 months old, n = 11) and aged (23-25 months old, n = 13) mice and sampled at 14 and 19 days. Angiogenic invasion was significantly delayed in aged mice at 14d relative to young at 14d (% area of invasion 9.0 ± 3.7 vs 19.0 ± 5.6; p = 0.02). Although microvessel morphology and basement membrane composition were similar between the age groups, a significant decrease in capillary density was noted in aged tissues at 14d (7.5 ± 4.1) and 19d (12.1 ± 2.8) relative to young at 14d (18.7 ± 2.3) ( p&lt;0.01 A14d vs Y14d). In comparison to young at 14d, the inflammatory response was decreased by 43 ± 2.9% and 36 ± 7.8% in aged mice at 14d and 19d, respectively. Tissues of aged mice showed less newly deposited collagen. There was a lack of expression of transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor (VEGF) in aged mice at 14d (0.63 ± 0.3) and 19d (1.14 ± 0.5) vs young at 14d (1.92 ± 0.5) (p≤0.01 A14d vs Y14d for VEGF). However, similar production of VEGF receptor2 was observed. In contrast to young mice, there was significantly increased expression of thrombospondin-2 (TSP-2) in aged mice from 14d (14.6 × 10 3  ± 7.3 × 10 3 ) to 19d (34.9 × 10 3  ± 17 × 10 3 ). We conclude that angiogenesis in aging is not merely delayed, but is altered due to multiple impairments.

journal of histochemistry and cytochemistry/the journal of histochemistry and cytochemistry

Impaired Angiogenesis in Aging Is Associated with Alterations in Vessel Density, Matrix Composition, Inflammatory Response, and Growth Factor Expression