Skip to main content
Wiley Open Access Collection logoLink to Wiley Open Access Collection
. 2021 Sep 10;290(6):1278. doi: 10.1111/joim.13365

Corrigendum

PMCID: PMC9050100  PMID: 34506682

In (1) the figure 2D data on the accumulation of cholesterol esters upon oxLDL challenge in monocyte‐derived macrophages carrying different genotypes in perilipin‐2 (PLIN2) are presented. The figure indicates that N is 8 and 9 for Ser251 and Pro251, respectively. While this is absolutely accurate, the ambiguity that was discovered was that for Ser251 this N = 8 does not originate from 8 unique individuals, but 8 measurements originating from 4 individuals (in the case of Pro251 we indeed present data from 9 unique individuals). The strength of this study is its recruit‐by‐ genotype design, however, it does also come with limitations; recruiting individuals by genotype and isolating monocytes for differentiation means that we can never foresee the yield of cells from these processes. In addition, these individuals were rigorously matched based on other polymorphisms in the locus, they were all male and the same age to reduce the risk of ‘pleiotropy’ and confounding of other characteristics. This unfortunately resulted in our inability of including more unique individuals in the Ser251 in figure 2D. Re‐analysing the data considering the median cholesterol ester measurement for each individual (where there are multiple measurements) instead of presenting all measurements (this resulting in N of 4 and 9, respectively), we obtain a borderline significance (p = 0.056 using a student's t‐test after Shapiro‐Wilk's test for normality) for the difference between Ser251 vs Pro251 in the oxLDL condition as shown in the revised figure 2D (for comparison, in the published figure p = 0.01). In univariate regression analyses of the effect the genotype and treatment on cholesterol esters, the effect of the genotype still achieves statistical significance (p = 0.03 Ser vs Pro), whereas the treatment and treatment‐ genotype interaction remain insignificant, which is in line with what we have published. Other figures including data from the monocyte‐derived macrophages have been re‐checked and are correctly stated. It is the authors’ opinion that this result does not change the data presented in the paper, nor any conclusions drawn. We apologize for this error.

Reference

  • 1. Saliba‐Gustafsson P et al., Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed‐ forward loop between LXR and autophagy. J Intern Med. 2019 Dec;286(6):660‐675. 10.1111/joim.12951 [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Journal of Internal Medicine are provided here courtesy of Wiley

RESOURCES