There was a mistake in Figure 2C as published. During preparation of the composite figure, the hydroxycobalamin (B12a) proliferation time-course plot in Figure 2C was inadvertently replaced with a copy of the hydroxychloroquine (HCQ) time-course plot from Figure 2F. The underlying experiments involved different compounds and the published time-course graphs should not have been identical.
Endogenous cyanide generation supports endothelial cell proliferation, migration and differentiation. (A) Detection of cyanide generation by the electrochemical method and (B) confocal microscopy using the cyanide-specific probe CSP in HUVECs incubated with or without VEGF for 72h. Effect of cyanide scavenger Vitamin B12a (B12a) (C–E) or hydroxychloroquine (HCQ) (F–H) in HUVECs in the presence of absence of 20 ng/mL VEGF on (C,F) cell proliferation, (D,G) wound healing, and (L,H) ATP production. Data are presented as mean ± SEM. Individual data points represent independent biological replicates. Statistical analysis was performed as described in the Materials and Methods section; significance is indicated as follows: *p < 0.05, **p < 0.01, ***p < 0.001.
Scientific figure presenting bar graphs, line graphs, and fluorescence microscopy images comparing cellular responses with and without VEGF treatment. Panel A shows VEGF increases cyanide production. Panel B displays increased CSP fluorescence in the +VEGF group with merged red and green channels, quantified in a bar graph. Panels C-H show proliferation, wound confluence, and ATP production with treatments B12a or HCQ, demonstrating VEGF-dependent increases, with statistical significance indicated.
An additional compilation error was identified in the deposited Figure 2C area-under-the-curve (AUC) data: in each of the four experimental groups, one replicate had been entered twice. The correct values for the affected replicates and the B12a time courses were recovered from the experiment-specific GraphPad Prism records. We have reconstructed Figure 2C using five distinct biological experiments per condition. The treatment headers in the original Figure 2C source-data file, which incorrectly referred to HCQ rather than B12a, will also be corrected.
The corrected mean AUC values for 0 and 10 µM B12a were 1428 and 1332 without VEGF, and 2229 and 2006 with VEGF, respectively. Analysis of the matched experiments confirms a significant inhibitory effect of B12a on VEGF-stimulated proliferation (adjusted p < 0.05). In the corrected graph the annotation for this comparison is * rather than **. The errors in Figure 2C do not change the principal conclusions of the article.
The corrected Figure 2 appears below. The correction concerns only the 2C part.
The original version of this article has been updated.
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