Fig 1: IGFBP-1 expression and pathological angiogenesis. (A,B) Mice with IGFBP-1 knock down were used to investigate recovery from hind limb ischemia as a model of pathological angiogenesis. (A) Representative laser Doppler perfusion images of mouse hind limbs on day 0, 7, and 14 after injury. (B) Quantitative analysis of the perfusion recovery measured by laser Doppler. The index was calculated as the ratio of ischemic to nonischemic hind limb perfusion. There is no difference in IGFBP-1-KO mice compared with wild-type litter mate controls There was no difference in necrotic toes between the genotypes (data not shown). N = 6 to 8 per group. (C,D) Mice overexpressing hIGFBP-1 were used to investigate recovery from hind limb ischemia. (C) Representative laser Doppler blood perfusion images of mouse hind limbs on day 0, 7, and 14 after injury. (D) Quantitative analysis of the perfusion recovery measured by laser Doppler. The index was calculated as the ratio of ischemic to non-ischemic hind limb blood perfusion. There was no difference in necrotic toes between the genotypes (data not shown) N = 7.
Fig 2: IGFBP-1 expression and developmental angiogenesis. (A–G) Retinas from IGFBP-1-KO mice p5 and wild-type litter mate controls were used to investigate the effects of IGFBP-1 knockout on developmental retinal angiogenesis. (A) Representative whole mount images. (B) There was no difference in vascular outgrowth (IGFBP-1-KO 1201 ± 165.4 V Wt 1248 ± 62.55), (C) vessel density (IGFBP-1-KO 30.4 ± 5 V Wt 31.5 ± 3.2), or (D) branching complexity (IGFBP-1-KO 38.6 ± 3.2 V Wt 37.8 ± 6) between IGFBP-1-KO mice and wild-type litter mate controls. (E) Representative images of vascular front of retinas from IGFBP-1-KO mice and wild-type litter mate controls. (F) There is no difference between tip cell number (IGFBP-1-KO 2.3 ± 0.34 V Wt 2.1 ± 0.1) or (G) number of filopodia (IGFBP-1-KO 10.7 ± 0.95 V Wt 9.3 ± 1. 78) between IGFBP-1-KO mice and wild-type litter mate controls (N = 4–5 per group). (H–N) Retinas from hIGFBP-1 overexpressing mice and wildtype litter mate controls were used to investigate the effects of hIGFBP-1 overexpression on retinal angiogenesis. (H) Representative whole mount images. (I) There is no difference in vascular outgrowth between IGFBP-1-tg mice and wildtype litter mate controls (tg 1579 ± 58.4 V Wt 1456 ± 55.6). (J) There is no difference in vessel density between IGFBP-1-tg mice and wild-type litter mate controls (tg 24.3 ± 2 V Wt 23.9 ± 1.4). (K) There is no difference in branching complexity between IGFBP-1-tg mice and wild-type litter mate controls (tg 28.4 ± 2.3 V Wt 31 ± 2.2). (L) Representative vascular front images. (M) There is no difference between tip cell number between IGFBP-1-tg mice and wild-type litter mate controls (tg 2 ± 0.18 V Wt 2.1 ± 0.21). (N: There is an increase in number of filopodia (white arrow head) in IGFBP-1-tg mice when compared with wild-type litter mate controls (tg 13 ± 1.1 V Wt 8 ± 0.66). N = 5 to 7 per group. Data are presented as mean ± SEM.
Supplier Page from Abcam for Mouse IGFBP-1 ELISA Kit