PR39, a peptide regulator of angiogenesis

Jian Li, Mark Post, Rudiger Volk, Youhe Gao, Min Li, C aroline Metais, Kaori Sato, Jo T sai, William Aird, Robert D. Rosenberg , Thomas G. Hampton, Jianyi Li, F rank Sellke, Peter Carmeliet & Michael Simons

Nature Medicine 6, 49– 55 (2000).

On page 51, Fig. 2a,c and d should be as presented here:

Fig. 2 PR39 induces HIF-1α and HIF-1α-dependent gene expression. a, HIF-1α protein levels in ECV cells cultured in normoxic (ECV) or hypoxic conditions (ECV Hypoxia) or stably transfected with the PR39 expression construct (ECV–PR39). Proteins immunoprecipitated with an antibody against HIF-1α were assessed by western blot analysis with an antibody against HIF-1α. There is increased HIF-1α expression in hypoxic ECV and PR39-transfected cells. c, Western blot analysis of VEGF (top) and NOS3 (eNOS; bottom) in ECV cells cultured for 24 h in the absence (−) or presence (+) of 1 μM PR39, or in the ECV–PR39 cell line. d, Northern blot analysis of VEGF and FGFR1 levels in PR39-treated bovine aortic endothelial cells, showing a dose-dependent response.

On page 52, Fig. 3c should be as presented here:

Fig. 3 c, Quantitative morphometric analyses of microvessels in αMHC–PR39 mice (right) and control mice (left); *, P<0.001, compared with control.

On page 53, Fig. 5b should be as presented here:

Fig. 5 Physiologic evaluation of PR39-induced angiogenesis b, Analysis of microvessels from αMHC–PR39 mice (▪) and control mice (▴), showing similar vessel reactivity to the endothelium-dependent vasodilator A23187 (left) and the smooth muscle relaxant sodium nitroprusside (SNP; right).

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