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. 2004 Jun 21;101(26):9833–9838. doi: 10.1073/pnas.0400337101

Fig. 4.

Fig. 4.

Local IGF-I is required for lesion-induced angiogenesis. (A) LID mice receiving a s.c. anti-IGF-I infusion simultaneously to the lesion show a significantly diminished increase in VEGF levels 3 days after the lesion, compared with control injured animals receiving either NRS infusion or saline. The upper gel shows a representative VEGF blot. The lower gel shows the PI3K blot for control of protein load. Histograms indicate quantitation of VEGF levels in the perilesion area (**, P < 0.01 vs. NRS and saline-treated brain injured mice; n = 4). (B) Similar results are found in peak HIF-1α levels 3 days after injury in anti-IGF-I-treated LID mice. The upper gel shows the HIF-1α blot, and the lower gel shows the protein load control with PI3K. Histograms show that HIF-1α is significantly diminished in the anti-IGF-I group (**, P < 0.01 vs. NRS and saline treated; n = 5). (C) Lectin immunocytochemistry of the perilesioned site indicates prominent vessel growth after 1 month of stab injury in saline-treated LID mice, whereas after infusion of anti-IGF-I, angiogenesis is absent. The white arrow indicates the position of the cannula tract. (Scale bar = 100 μm.) (D) Vessel density in the perilesion area increases in saline-treated and NRS-treated LID mice, compared with sham-operated animals, but not in injured anti-IGF-I-treated LID mice (***, P < 0.001 vs. NRS and saline treated; n = 4 per group).