Correction

BK Ambati, E Patterson, P Jani, et al. Soluble vascular endothelial growth factor receptor-1 contributes to the corneal antiangiogenic barrier. Br J Ophthalmol 2007;91:505–8.

Figures 4 and 8 were erroneous submissions; the correct figures are available online. Lane 1 and the marker lane of fig 8 duplicate those of fig 4. This resulted from the fact that, during the editing process, the authors were asked to provide two separate figures demonstrating, firstly, that sFlt binds VEGF in normal human cornea (fig 4), and secondly, that in neovascularised specimens binding of sFlt to VEGF is reduced relative to normal (fig 8). This does not alter the conclusions that sFlt binds VEGF and that there is reduced binding in the disease state. Also, the molecular weight in fig 8 in the original paper was mislabelled as 25 kD rather than 46 kD. Although the gel was run under reducing conditions, for reasons unclear to the angiogenesis field, the migration of VEGF species extracted from tissues, even under reducing conditions, is known to be anomalous as it often migrates around 46 kD, suggesting a secondary/tertiary structure of the VEGF dimer that is resistant to complete reduction as noted by other investigators (Kallapur SG, et al. Am J Physiol Lung Cell Mol Physiol 2004;287:L1178–85; Tee MK and Jaffe RB. Biochem J 2001;359:219–26; Jingjing L, et al. Mol Cell Biochem 2000;214:23–30).

Figure 5 erroneously duplicated bands in fig 3. The correct Western blots demonstrating reduced/absent sFlt in neovascularised human corneas compared with normal corneas are available online; these data are from experiments performed prior to the earlier incorrectly presented data.

It should also be noted that the original fig 7B is a reproduction of fig 4D in an earlier paper of ours (Ambati, et al. Nature 2006;443:993–7), which was reference 4 in our paper. In this paper, we showed it as an example of reduced sFlt expression in a condition associated with corneal neovascularisation in humans. In the earlier paper we showed it as an example of Pax6 mutations in aniridia being associated with decreased sFlt in humans. We now show several other examples of aniridic human corneas with low levels of sFlt expression, reinforcing our conclusion that aniridic corneal neovascularisation is associated with low sFlt levels. Nonetheless, the published guidelines of both Nature and Br J Ophthalmol accord with reuse of an earlier figure.

The authors regret the oversights that led to these errors of assembly and editing. Although these mistakes do not alter the conclusions of the article, the authors wish to inform other scientists of these problems and provide an accurate representation of their work.