Erratum

Corrigendum to “Plasmalogen modulation attenuates atherosclerosis in ApoE- and ApoE/GPx1-deficient mice” (Atherosclerosis (2015) 243(2) (598–608) (S0021915015301805) (10.1016/j.atherosclerosis.2015.10.096))

Aliki A. Rasmiena, Christopher K. Barlow, Nada Stefanovic, Kevin Huynh, Ricardo Tan, Arpeeta Sharma, Dedreia Tull, Judy B. de Haan, Peter J. Meikle

Research output: Contribution to journalComment / DebateOtherpeer-review

Abstract

The authors regret the published article contains an error in the quantification of the lysophospholipid species. The relative levels of sn-1 and sn-2 LPC and LPE in both plasma and heart of the untreated and BA-treated animals were misrepresented in Fig. 2. A correct version of Fig. 2 is now provided. The changes in the figure have not altered the interpretation in the manuscript with respect to the atherosclerosis outcome or to the increase in sn-2 LPC in the BA-treated animals that was likely due to the oxidation of plasmalogen. Rather, this figure provides a more accurate representation of the relative level of sn-1 and sn-2 species of LPC and LPE in plasma and heart. Further, in section 3.3 page 601, we stated “We observed a significantly higher level (P < 0.05) of LPC and LPE in plasma and heart of all the BA-treated mouse groups (data not shown).” Our reanalysis has shown this statement to be in error and should be corrected with the following: “We observed a higher level of LPC (P < 0.05) relative to total PC in plasma of BA-treated ApoE−∖− and a lower level in the treated C57/BL6 compared to the untreated groups of the same genotypes. LPE relative to total PC was higher in the plasma of the BA-treated ApoE−∖−GPx1−/− only, compared to the untreated group. In addition, we observed a higher level of LPE (P < 0.05) in heart of all the BA-treated mouse groups relative to the untreated control groups of the same genotypes (data not shown).” Fig. 2. Level of lysophosphatidylcholine and lysophosphatidylethanolamine in plasma and heart of mice following 12 weeks of high fat diet supplemented with/without batyl alcohol. Total level of sn-1 and sn-2 lysophosphatidylcholine (sn-1 LPC and sn-2 LPC, respectively), and sn-1 and sn-2 lysophosphatidylethanolamine (sn-1 LPE and sn-2 LPE, respectively) in (A and B) plasma; and (C and D) heart of C57/BL6 (N = 10), ApoE−∖− (N = 10), and ApoE−∖−GPx1−/− (N = 9) mice on high fat diet supplemented with either 0% batyl alcohol (open bars) or 2% batyl alcohol (closed bars). Bars indicate median, whiskers indicate interquartile range. The two dietary groups of each genotype were analysed using Mann–Whitney U-test; * indicates P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001. The authors would like to apologise for any inconvenience caused.

Original languageEnglish
Pages (from-to)314-315
Number of pages2
JournalAtherosclerosis
Volume254
DOIs
Publication statusPublished - 1 Nov 2016
Externally publishedYes

Cite this

@article{ef1221e8151d468e8147dd2273c35222,
title = "Erratum: Corrigendum to “Plasmalogen modulation attenuates atherosclerosis in ApoE- and ApoE/GPx1-deficient mice” (Atherosclerosis (2015) 243(2) (598–608) (S0021915015301805) (10.1016/j.atherosclerosis.2015.10.096))",
abstract = "The authors regret the published article contains an error in the quantification of the lysophospholipid species. The relative levels of sn-1 and sn-2 LPC and LPE in both plasma and heart of the untreated and BA-treated animals were misrepresented in Fig. 2. A correct version of Fig. 2 is now provided. The changes in the figure have not altered the interpretation in the manuscript with respect to the atherosclerosis outcome or to the increase in sn-2 LPC in the BA-treated animals that was likely due to the oxidation of plasmalogen. Rather, this figure provides a more accurate representation of the relative level of sn-1 and sn-2 species of LPC and LPE in plasma and heart. Further, in section 3.3 page 601, we stated “We observed a significantly higher level (P < 0.05) of LPC and LPE in plasma and heart of all the BA-treated mouse groups (data not shown).” Our reanalysis has shown this statement to be in error and should be corrected with the following: “We observed a higher level of LPC (P < 0.05) relative to total PC in plasma of BA-treated ApoE−∖− and a lower level in the treated C57/BL6 compared to the untreated groups of the same genotypes. LPE relative to total PC was higher in the plasma of the BA-treated ApoE−∖−GPx1−/− only, compared to the untreated group. In addition, we observed a higher level of LPE (P < 0.05) in heart of all the BA-treated mouse groups relative to the untreated control groups of the same genotypes (data not shown).” Fig. 2. Level of lysophosphatidylcholine and lysophosphatidylethanolamine in plasma and heart of mice following 12 weeks of high fat diet supplemented with/without batyl alcohol. Total level of sn-1 and sn-2 lysophosphatidylcholine (sn-1 LPC and sn-2 LPC, respectively), and sn-1 and sn-2 lysophosphatidylethanolamine (sn-1 LPE and sn-2 LPE, respectively) in (A and B) plasma; and (C and D) heart of C57/BL6 (N = 10), ApoE−∖− (N = 10), and ApoE−∖−GPx1−/− (N = 9) mice on high fat diet supplemented with either 0{\%} batyl alcohol (open bars) or 2{\%} batyl alcohol (closed bars). Bars indicate median, whiskers indicate interquartile range. The two dietary groups of each genotype were analysed using Mann–Whitney U-test; * indicates P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001. The authors would like to apologise for any inconvenience caused.",
author = "Rasmiena, {Aliki A.} and Barlow, {Christopher K.} and Nada Stefanovic and Kevin Huynh and Ricardo Tan and Arpeeta Sharma and Dedreia Tull and {de Haan}, {Judy B.} and Meikle, {Peter J.}",
year = "2016",
month = "11",
day = "1",
doi = "10.1016/j.atherosclerosis.2016.01.046",
language = "English",
volume = "254",
pages = "314--315",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier",

}

Erratum : Corrigendum to “Plasmalogen modulation attenuates atherosclerosis in ApoE- and ApoE/GPx1-deficient mice” (Atherosclerosis (2015) 243(2) (598–608) (S0021915015301805) (10.1016/j.atherosclerosis.2015.10.096)). / Rasmiena, Aliki A.; Barlow, Christopher K.; Stefanovic, Nada; Huynh, Kevin; Tan, Ricardo; Sharma, Arpeeta; Tull, Dedreia; de Haan, Judy B.; Meikle, Peter J.

In: Atherosclerosis, Vol. 254, 01.11.2016, p. 314-315.

Research output: Contribution to journalComment / DebateOtherpeer-review

TY - JOUR

T1 - Erratum

T2 - Corrigendum to “Plasmalogen modulation attenuates atherosclerosis in ApoE- and ApoE/GPx1-deficient mice” (Atherosclerosis (2015) 243(2) (598–608) (S0021915015301805) (10.1016/j.atherosclerosis.2015.10.096))

AU - Rasmiena, Aliki A.

AU - Barlow, Christopher K.

AU - Stefanovic, Nada

AU - Huynh, Kevin

AU - Tan, Ricardo

AU - Sharma, Arpeeta

AU - Tull, Dedreia

AU - de Haan, Judy B.

AU - Meikle, Peter J.

PY - 2016/11/1

Y1 - 2016/11/1

N2 - The authors regret the published article contains an error in the quantification of the lysophospholipid species. The relative levels of sn-1 and sn-2 LPC and LPE in both plasma and heart of the untreated and BA-treated animals were misrepresented in Fig. 2. A correct version of Fig. 2 is now provided. The changes in the figure have not altered the interpretation in the manuscript with respect to the atherosclerosis outcome or to the increase in sn-2 LPC in the BA-treated animals that was likely due to the oxidation of plasmalogen. Rather, this figure provides a more accurate representation of the relative level of sn-1 and sn-2 species of LPC and LPE in plasma and heart. Further, in section 3.3 page 601, we stated “We observed a significantly higher level (P < 0.05) of LPC and LPE in plasma and heart of all the BA-treated mouse groups (data not shown).” Our reanalysis has shown this statement to be in error and should be corrected with the following: “We observed a higher level of LPC (P < 0.05) relative to total PC in plasma of BA-treated ApoE−∖− and a lower level in the treated C57/BL6 compared to the untreated groups of the same genotypes. LPE relative to total PC was higher in the plasma of the BA-treated ApoE−∖−GPx1−/− only, compared to the untreated group. In addition, we observed a higher level of LPE (P < 0.05) in heart of all the BA-treated mouse groups relative to the untreated control groups of the same genotypes (data not shown).” Fig. 2. Level of lysophosphatidylcholine and lysophosphatidylethanolamine in plasma and heart of mice following 12 weeks of high fat diet supplemented with/without batyl alcohol. Total level of sn-1 and sn-2 lysophosphatidylcholine (sn-1 LPC and sn-2 LPC, respectively), and sn-1 and sn-2 lysophosphatidylethanolamine (sn-1 LPE and sn-2 LPE, respectively) in (A and B) plasma; and (C and D) heart of C57/BL6 (N = 10), ApoE−∖− (N = 10), and ApoE−∖−GPx1−/− (N = 9) mice on high fat diet supplemented with either 0% batyl alcohol (open bars) or 2% batyl alcohol (closed bars). Bars indicate median, whiskers indicate interquartile range. The two dietary groups of each genotype were analysed using Mann–Whitney U-test; * indicates P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001. The authors would like to apologise for any inconvenience caused.

AB - The authors regret the published article contains an error in the quantification of the lysophospholipid species. The relative levels of sn-1 and sn-2 LPC and LPE in both plasma and heart of the untreated and BA-treated animals were misrepresented in Fig. 2. A correct version of Fig. 2 is now provided. The changes in the figure have not altered the interpretation in the manuscript with respect to the atherosclerosis outcome or to the increase in sn-2 LPC in the BA-treated animals that was likely due to the oxidation of plasmalogen. Rather, this figure provides a more accurate representation of the relative level of sn-1 and sn-2 species of LPC and LPE in plasma and heart. Further, in section 3.3 page 601, we stated “We observed a significantly higher level (P < 0.05) of LPC and LPE in plasma and heart of all the BA-treated mouse groups (data not shown).” Our reanalysis has shown this statement to be in error and should be corrected with the following: “We observed a higher level of LPC (P < 0.05) relative to total PC in plasma of BA-treated ApoE−∖− and a lower level in the treated C57/BL6 compared to the untreated groups of the same genotypes. LPE relative to total PC was higher in the plasma of the BA-treated ApoE−∖−GPx1−/− only, compared to the untreated group. In addition, we observed a higher level of LPE (P < 0.05) in heart of all the BA-treated mouse groups relative to the untreated control groups of the same genotypes (data not shown).” Fig. 2. Level of lysophosphatidylcholine and lysophosphatidylethanolamine in plasma and heart of mice following 12 weeks of high fat diet supplemented with/without batyl alcohol. Total level of sn-1 and sn-2 lysophosphatidylcholine (sn-1 LPC and sn-2 LPC, respectively), and sn-1 and sn-2 lysophosphatidylethanolamine (sn-1 LPE and sn-2 LPE, respectively) in (A and B) plasma; and (C and D) heart of C57/BL6 (N = 10), ApoE−∖− (N = 10), and ApoE−∖−GPx1−/− (N = 9) mice on high fat diet supplemented with either 0% batyl alcohol (open bars) or 2% batyl alcohol (closed bars). Bars indicate median, whiskers indicate interquartile range. The two dietary groups of each genotype were analysed using Mann–Whitney U-test; * indicates P < 0.05, ** indicates P < 0.01 and *** indicates P < 0.001. The authors would like to apologise for any inconvenience caused.

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U2 - 10.1016/j.atherosclerosis.2016.01.046

DO - 10.1016/j.atherosclerosis.2016.01.046

M3 - Comment / Debate

VL - 254

SP - 314

EP - 315

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

ER -