Correction Volume 13, Issue 14 pp 19078—19079
Correction for: Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
- 1 Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang, 550002, P. R. China
- 2 Department of Cardiology, The General Hospital of Ji’nan Military Region, Ji’nan, 250031, P. R. China
- 3 Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA
Received: July 19, 2021 Accepted: July 31, 2021 Published: July 31, 2021https://doi.org/10.18632/aging.203391
How to Cite
Copyright: © 2021 Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This article has been corrected: The authors replaced the “oe-H19 + oe-CTCF + oe-PKD1” panel of the HE staining in Figure 5C, which was accidently mislabeled and partially duplicated with the “oe-NC + oe-NC + oe-NC” image. Replacement was done using representative images from the original sets of experiments. This alteration does not affect the results or conclusions of this work.
The new Figure 5 is presented below.
Figure 5. H19 is involved in atherosclerotic vulnerable plaque formation and intraplaque angiogenesis through down-regulating PKD1 by recruiting CTCF in ApoE knockout mice with AS. (A) The expression pattern of PKD1 in the aortic tissues of normal and AS mice determined by RT-qPCR. * p < 0.05 vs. the control group. (B) The overexpressing efficiency of H19, CTCF and PKD1 assessed by RT-qPCR. * p < 0.05 vs. the oe-NC + oe-NC + oe-NC group; # p < 0.05 vs. the oe-H19 + oe-CTCF + oe-NC group. (C) The atherosclerotic vulnerable plaque formation evaluated by HE staining (× 400) (The arrow referred to lipid vacuoles, * represented inflammatory cells and # indicated fractured smooth muscle). (D) The number of new blood vessels measured by Immunohistochemical staining (× 400) (The arrow referred to CD34-positive cells). (E) The protein levels of MMP-2, VEGF, p53 and TIMP-1 in atherosclerotic plaques normalized to GAPDH after transfection determined by Western blot analysis. * p < 0.05 vs. the oe-NC + oe-NC + oe-NC group. The data were measurement data and expressed by mean ± standard deviation. Data differences between two groups were analyzed by unpaired t-test; comparisons made among multiple groups were analyzed by one-way ANOVA. The experiments were repeated three times independently.