ABSTRACT
Following the publication of the above paper, a concerned reader drew to the Editor's attention that the "con" and "oxLDL" panels in Fig. 1E on p. 3602, and various data panels included in Figs. 3 and 5 on p. 3604, contained apparent anomalies, including what appeared to be matching patternings of cellular data either within the same figure panels or comparing among the data panels. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence in the overall authenticity of the data. After having consulted the authors in this regard, they agreed with the decision to retract this paper. The Editor deeply regrets any inconvenience that has been caused to the readership of the Journal. [Molecular Medicine Reports 12: 35993606, 2015; DOI: 10.3892/mmr.2015.3864.
ABSTRACT
Oxidized lowdensity lipoprotein (oxLDL) can increase the expression of adipophilin and the accumulation of intracellular lipid droplets. However, the detailed mechanisms remain to be fully elucidated. The present study aimed to investigate the mechanism underlying the effect of oxLDL on the expression of adipophilin and the accumulation of intracellular cholesterol esters. The results revealed that oxLDL increased the activation of protein kinase C α (PKCα), expression of adipophilin and acylcoenzymeA: cholesterol acyltransferse 1 (ACAT1) and increased accumulation of intracellular cholesterol esters. In addition, PKCα siRNA abrogated oxLDLinduced adipophilin, expression of ATAC1 and accumulation of cholesterol esters. Furthermore, oxLDL increased the accumulation of intracellular cholesterol esters and expression of ACAT1, and this effect were reversed by transfection with adipophilin siRNA. Taken together, these results demonstrated that oxLDL induces the accumulation of cholesterol esters, which is mediated by the PKCαadipophilinACAT1 pathway.
