Jci_page_head_homepage_01 Jci_page_head_homepage_02
Article tools
  • View PDF
  • Cite this article
  • E-mail this article
  • Share this article
  • Send a letter
  • Information on reuse
  • Standard abbreviations
Author information
Need help?

Erratum

Genetic inactivation of IL-1 signaling enhances atherosclerotic plaque instability and reduces outward vessel remodeling in advanced atherosclerosis in mice

Matthew R. Alexander, Christopher W. Moehle, Jason L. Johnson, Zhengyu Yang, Jae K. Lee, Christopher L. Jackson and Gary K. Owens

Published February 1, 2012

Original citation: J. Clin. Invest. 2012;122(1):70–79. doi:10.1172/JCI43713.

Citation for this erratum: J. Clin. Invest. 2012;122(2):783. doi:10.1172/JCI62827.

During the preparation of this manuscript, errors were inadvertently introduced into the legends for Figures 1, 2, and 3. The correct sections of the legends appear below.

Figure 1: (B) Quantification of total atherosclerotic plaque area within the aortic root of Il1r1+/+Apoe–/– and Il1r1–/–Apoe–/– mice at 150-μm intervals from the aortic valve attachment site (P < 0.001 for difference between genotypes by Scheirer-Ray-Hare test). n = 13, Il1r1+/+Apoe–/–; n = 12, Il1r1–/–Apoe–/–. Data represent mean ± SEM.

Figure 2: L-1R1 deficiency reduces compensatory outward remodeling of atherosclerotic brachiocephalic arteries. (A) Movat staining of representative brachiocephalic arteries of Il1r1–/–Apoe–/– and Il1r1+/+Apoe–/– mice. Scale bars: 200 μm. (BD) Atherosclerotic plaque area (B), vessel area within the IEL (P < 0.001 for difference between genotypes by 2-way ANOVA) (C), and lumen area (P < 0.001 for difference between genotypes by 2-way ANOVA after square root transformation) (D) at multiple locations along the brachiocephalic arteries of Il1r1–/–Apoe–/– and Il1r1+/+Apoe–/– mice. n = 14, Il1r1+/+Apoe–/–; n = 12, Il1r1–/–Apoe–/–. Data in BD represent mean ± SEM.

Figure 3: (FJ) Quantification of (F) plaque collagen content based on picrosirius red staining, P < 0.001 for difference of genotypes by 2-way ANOVA, (G) plaque SMC coverage based on SM α-actin staining, P < 0.001 for difference of genotypes by the Scheirer-Ray-Hare test, (H) total plaque SMC content based on SM α-actin staining, P < 0.001 for difference of genotypes by the Scheirer-Ray-Hare test, (I) plaque macrophage content based on Mac2 staining, P = 0.01 for difference of genotypes by 2-way ANOVA after log transformation, and (J) the percentage of brachiocephalic arteries exhibiting intraplaque hemorrhage based on Movat and TER-119 staining, **P < 0.01 by Fisher’s exact test.

The JCI regrets the error.