Hypermethylation of the Micro-RNA 145 Promoter Is the Key Regulator for NLRP3 Inflammasome-Induced Activation and Plaque Formation
J Am Coll Cardiol Basic Trans Science 2018;3:604-24.
Wei Zhong, PhD, Bo Li, MD, Yao Xu, MD, Ping Yang, MD, Rui Chen, PhD, Zhongqun Wang, PhD, Chen Shao, MD, Juan Song, PhD, Jinchuan Yan, MD, PhD
In the above article, Figures 4 and 6 have been replaced due to the following errors.
Figure 4.
Methylation of the miR-145 Promoter Was Mediated by DNMT1 and Tet2 Dynamic Alteration
(A and B) DNMT1 knockdown or Tet2 overexpression efficiency and the effect on miR-145 expression in vascular smooth muscle cells treated with TNF-α. Values are mean ± SEM of 3 samples in each group; ∗p < 0.05. (C) Methylation-specific polymerase chain reaction of the +129 CpG site in vascular smooth muscle cells treated with TNF-α with knockdown of DNMT1 or overexpression of Tet2. The methylated specific bands were obvious in the sh-con or Plenti-con groups treated with TNF-α, whereas the unmethylated specific bands were obvious in the sh-DNMT1 + TNF-α group and Plenti-Tet2 + TNF-α group. (D) Chromatin immunoprecipitation assay identified the miR-145 promoter sequence binding with DNMT1 and Tet2. (E) The relative enrichment rate of the chromatin immunoprecipitation assay was determined by reverse transcription polymerase chain reaction. Values are mean ± SEM of 3 samples in each group; ∗p < 0.05 vs. the con group. IgG = immunoglobulin G; mRNA = messenger ribonucleic acid; sh- = small hairpin RNA targeting; other abbreviations as in Figures 2 and 3.
Figure 6.
MiR-145 Inhibited NLRP3 Inflammasome Activation Induced by TNF-α in Vascular Smooth Muscle Cells
(A and B) Western blot and quantitative results of NLRP3, pro-IL-1β, and mature IL-1β in vascular smooth muscle cells treated with TNF-α and the miR-145 mimic (100 nmol/l). Values are mean ± SEM of 3 samples in each group; ∗p < 0.05. (C and D) Western blot and quantitative results of NLRP3, pro-IL-1β, and mature IL-1β in vascular smooth muscle cells treated with 5-aza and the miR-145 inhibitor (100 nmol/l). Values are mean ± SEM of 3 samples in each group; ∗p < 0.05. (E) Concentration of IL-1β in supernatants of vascular smooth muscle cells with different treatments. Values are mean ± SEM of 3 samples in each group; ∗p < 0.05. (F) Immunofluorescence of IL-1β accumulation in vascular smooth muscle cells with different treatments. INC = inhibitor control; NC = mimic control; other abbreviations as in Figures 1 to 3 and 5.
In Figure 4, the original panel A mistakenly used the β-actin control lane from Figure 7A.
The Western blots for the right hand panel of Figure 4B have been repeated, and Figure 4B now has the correct β-actin loading control lane. The revised data are similar to the original Western blot and did not change the interpretation of the findings in the original submission.
In Figure 6, panel A mistakenly used the β-actin control lane from Figure 7A.
The experiments with smooth muscle cells in Figures 6A and 6B were repeated, and new Western blots were performed. Figure 6A now has the correct β-actin loading control lane. The group data for panel 6B have been calculated using the appropriate β-actin loading control lane. The revised data analysis is similar to the original analysis of the group data and did not change the original interpretation of the findings in the original submission.
The online version of the article has been corrected to reflect these changes.
The authors regret these errors.