Correction to: Scientific Reports https://doi.org/10.1038/s41598-020-58849-z, published online 10 February 2020
This Article contains a repeated error in the group of wildtype mice. The same group of wildtype mice was utilized as a comparison to multiple knockout models and presented the data across several figures. The baseline control images for these wildtype mice in healthy (referred to as dim-reared; DR) and diseased conditions (referred to as photo-oxidative damage (PD)), were used as a comparison to knockout models.
As a result of this error, the legends of Figure 1, 4 and 6,
Figure 1. “Caspase1/11−/− mice have better-preserved retinal function and reduced inflammation and cell death following photo-oxidative damage (PD) compared to WT controls. (A–D) Retinal function was measured before (DR) and after 5 days PD using ERG. Casp1/11−/− mice had significantly lower retinal function in DR conditions compared to WT controls, for both (A) a-wave and (B) b-wave responses (P < 0.05, N = 6). However, following 5 days PD, retinal function in Casp1/11−/− mice was significantly higher than WT PD controls for both (C) a-wave and (D) b-wave response (P < 0.05, N = 10). E-J The effect of Casp1/11 deficiency on photoreceptor cell death. Representative confocal images show ONL thickness and TUNEL+ cells in the ONL of (E) WT and (F) Casp1/11−/− mice following PD. (G) Casp1/11−/− mice has significantly fewer TUNEL+ cells in the ONL and (H) significantly more photoreceptor rows than WT PD controls (P < 0.05, N = 6). (I,J) There was no significant difference in ONL thickness between DR Casp1/11−/− mice and WT controls (P > 0.05, N = 6), however, after PD, the ONL of Casp1/11−/− mice was significantly thicker than WT PD controls (P < 0.05, N = 6). (K–P) The effect of Casp1/11 deficiency on inflammation in the retina following PD. Representative confocal images show an increased number of IBA-1+ microglia in (K) WT PD mice compared to fewer in (L) Casp1/11−/− PD mice. (M) Casp1/11−/− mice had significantly fewer IBA-1+ microglia in the outer retina than WT controls following PD (P < 0.05, N = 6). (N) Casp1/11−/− PD mice had a significantly reduced level of IL-1β protein as measured by ELISA than WT PD controls (P < 0.05, N = 6). (O) In addition, Casp1/11−/− PD mice has significantly reduced levels of IL-1β, IL-6 and CXCL1 compared to WT PD mice, (P < 0.05, N = 6). Scale bars = 50 μM. *WT controls used in Fig. 1 are the same as in Fig. 4, with all mice participating in the same experimental run.”
should read:
“Caspase1/11−/− mice have better-preserved retinal function and reduced inflammation and cell death following photo-oxidative damage (PD) compared to WT controls. (A–D) Retinal function was measured before (DR) and after 5 days PD using ERG. Casp1/11−/− mice had significantly lower retinal function in DR conditions compared to WT controls, for both (A) a-wave and (B) b-wave responses (P < 0.05, N = 6). However, following 5 days PD, retinal function in Casp1/11−/− mice was significantly higher than WT PD controls for both (C) a-wave and (D) b-wave response (P < 0.05, N = 10). WT controls used for functional analysis in Fig. 1 are the same as in Fig. 4, with mice participating in the same experimental run. E-J The effect of Casp1/11 deficiency on photoreceptor cell death. Representative confocal images show ONL thickness and TUNEL+ cells in the ONL of (E) WT and (F) Casp1/11−/− mice following PD. (G) Casp1/11−/− mice has significantly fewer TUNEL+ cells in the ONL and (H) significantly more photoreceptor rows than WT PD controls (P < 0.05, N = 6). (I,J) There was no significant difference in ONL thickness between DR Casp1/11−/− mice and WT controls (P > 0.05, N = 6), however, after PD, the ONL of Casp1/11−/− mice was significantly thicker than WT PD controls (P < 0.05, N = 6). (K–P) The effect of Casp1/11 deficiency on inflammation in the retina following PD. Representative confocal images show an increased number of IBA-1+ microglia in (K) WT PD mice compared to fewer in (L) Casp1/11−/− PD mice. (M) Casp1/11−/− mice had significantly fewer IBA-1+ microglia in the outer retina than WT controls following PD (P < 0.05, N = 6). (N) Casp1/11−/− PD mice had a significantly reduced level of IL-1β protein as measured by ELISA than WT PD controls (P < 0.05, N = 6). (O) In addition, Casp1/11−/− PD mice has significantly reduced levels of IL-1β, IL-6 and CXCL1 compared to WT PD mice, (P < 0.05, N = 6). Scale bars = 50 μM. *WT controls used in Fig. 1 are the same as in Fig. 4, and Fig 6, with mice participating in the same experimental run.”
Figure 4. “Nlrp3−/− mice show better-preservation of retinal function following PD compared to WT controls. (A–D) Retinal function was measured before (DR) and after 5 days PD using ERG. Nlrp3−/− mice had a small but significantly lower retinal function in DR conditions compared to WT controls, for both (A) a-wave and (B) b-wave (P < 0.05, N = 6). However, following 5 days PD, retinal function in Nlrp3−/− mice was significantly higher than WT PD controls for both (C) a-wave and (D) b-wave (P < 0.05, N = 8). (E–J) The effect of Nlrp3 deficiency on photoreceptor cell death. Representative confocal images show ONL thickness and TUNEL+ cells in the ONL of (E) WT PD and (F) Nlrp3−/− PD mice. (G) There was no significant difference in TUNEL+ cell counts in the ONL between Nlrp3−/− PD mice and WT controls (P > 0.05, N = 6). (H) Nlrp3−/− PD mice had a small but significant increase in photoreceptor rows than WT controls (P < 0.05, N = 8). (I,J) There was no significant difference in ONL thickness between Nlrp3−/− and WT controls for DR or PD groups (P > 0.05, N = 6). (K–P) The effect of Nlrp3 deficiency on inflammation in the retina following PD. Representative confocal images show IBA-1+ microglia in (K) WT PD mice compared to (L) Nlrp3−/− PD mice. (M) No significant difference in the number of IBA-1+ microglia were seen in the outer retina of Nlrp3−/− and WT PD mice (P > 0.05, N = 8). (N) No change was seen in retinal IL-1β protein levels as measured by ELISA between Nlrp3−/− and WT PD mice (P > 0.05, N = 6). Scale bars = 50 μM. *WT controls used in Fig. 1 are the same as in Fig. 4, with all mice participating in the same experimental run.”
should read:
“Nlrp3−/− mice show better-preservation of retinal function following PD compared to WT controls. (A–D) Retinal function was measured before (DR) and after 5 days PD using ERG. Nlrp3−/− mice had a small but significantly lower retinal function in DR conditions compared to WT controls, for both (A) a-wave and (B) b-wave (P < 0.05, N = 6). However, following 5 days PD, retinal function in Nlrp3−/− mice was significantly higher than WT PD controls for both (C) a-wave and (D) b-wave (P < 0.05, N = 8). WT controls used for functional analysis in Fig. 1 are the same as in Fig. 4, with mice participating in the same experimental run. (E–J) The effect of Nlrp3 deficiency on photoreceptor cell death. Representative confocal images show ONL thickness and TUNEL+ cells in the ONL of (E) WT PD and (F) Nlrp3−/− PD mice. (G) There was no significant difference in TUNEL+ cell counts in the ONL between Nlrp3−/− PD mice and WT controls (P > 0.05, N = 6). (H) Nlrp3−/− PD mice had a small but significant increase in photoreceptor rows than WT controls (P < 0.05, N = 8). (I,J) There was no significant difference in ONL thickness between Nlrp3−/− and WT controls for DR or PD groups (P > 0.05, N = 6). (K–P) The effect of Nlrp3 deficiency on inflammation in the retina following PD. Representative confocal images show IBA-1+ microglia in (K) WT PD mice compared to (L) Nlrp3−/− PD mice. (M) No significant difference in the number of IBA-1+ microglia were seen in the outer retina of Nlrp3−/− and WT PD mice (P > 0.05, N = 8). (N) No change was seen in retinal IL-1β protein levels as measured by ELISA between Nlrp3−/− and WT PD mice (P > 0.05, N = 6). Scale bars = 50 μM. *WT controls used in Fig. 1 are the same as in Fig. 4, with all mice participating in the same experimental run. *WT controls used in Fig. 1 are the same as in Fig. 4, and Fig 6, with mice participating in the same experimental run.”
Figure 6. “Casp11 − / − mice show no preservation of retinal function following PD. (A–D) Retinal function was measured before (DR) and after 5 days PD using ERG. There was no significant difference in retinal function between Casp11 − / − and WT mice, in DR conditions for (A) a-wave or (B) b-wave responses or for (C) a-wave or (D) b-wave responses following PD (P > 0.05, N = 6). (E–J) The effect of Casp-11 deficiency on photoreceptor cell death. (E,F) No significant difference in ONL thickness was seen between Casp11 − / − and WT mice for DR or PD groups (P > 0.05, N = 6). No significant difference was seen between Casp11 − / − and WT PD groups for (G) TUNEL + cell counts in the outer retina or in (H) photoreceptor row counts (P > 0.05, N = 6). Representative images show retinal thickness and TUNEL + cells in the ONL for (I) WT PD mice and (J) Casp11 − / − PD mice. (K,L) The effect of Casp-11 deficiency on inflammation in the outer retina following PD. (K) No significant difference was seen in total IBA-1 + cell counts in the outer retina following PD between Casp11 − / − and WT mice (P > 0.05, N = 6). Representative confocal images show IBA-1 + microglia in the outer retina of (L) WT PD and (M) Casp11 − / − mice. Scale bars = 50 μM.”
should read:
“Casp11−/− mice show no preservation of retinal function following PD. (A–D) Retinal function was measured before (DR) and after 5 days PD using ERG. There was no significant difference in retinal function between Casp11−/− and WT mice, in DR conditions for (A) a-wave or (B) b-wave responses or for (C) a-wave or (D) b-wave responses following PD (P>0.05, N=6). (E–J) The effect of Casp-11 deficiency on photoreceptor cell death. (E,F) No significant difference in ONL thickness was seen between Casp11−/− and WT mice for DR or PD groups (P>0.05, N=6). No significant difference was seen between Casp11−/− and WT PD groups for (G) TUNEL+ cell counts in the outer retina or in (H) photoreceptor row counts (P>0.05, N=6). Representative images show retinal thickness and TUNEL+ cells in the ONL for (I) WT PD mice and (J) Casp11−/− PD mice. (K,L) The effect of Casp-11 deficiency on inflammation in the outer retina following PD. (K) No significant difference was seen in total IBA-1+ cell counts in the outer retina following PD between Casp11−/− and WT mice (P>0.05, N=6). Representative confocal images show IBA-1+ microglia in the outer retina of (L) WT PD and (M) Casp11−/− mice. Scale bars=50μM.*WT controls used in Fig. 1 are the same as in Fig. 4 and Fig 6, with mice participating in the same experimental run.”
Additionally, the Article contains the same error in Supplementary Figure 1, 2 and 3 legends, where wildtype mice were again used in multiple figures reflecting that they were the same controls. As the result, “*WT controls used in Supplementary Fig. 2 include mice from the same experimental group as in Supplementary Fig 1 and 3.” should be added to the Supplementary Figure 1, 2 and 3 legends.
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Wooff, Y., Fernando, N., Wong, J.H.C. et al. Author Correction: Caspase-1-dependent inflammasomes mediate photoreceptor cell death in photo-oxidative damage-induced retinal degeneration. Sci Rep 14, 21585 (2024). https://doi.org/10.1038/s41598-024-71519-8
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DOI: https://doi.org/10.1038/s41598-024-71519-8