Retracted : Advanced glycation end‚Äêproducts induce oxidative stress through the Sirt1/Nrf2 axis by interacting with the receptor of AGEs¬†under diabetic conditions
Authors: Xiao-Hua Gong
Qi Zhou
Jin-Ping Jie
Wen-Jun Wu
Xiong Chen
Fang Wang
Xiao-Jun Chen
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NF-E2-related factor 2; advanced glycation end-products; diabetes mellitus; oxidative stress; receptor for advanced glycation end products, sirtuin1
Affiliations: Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China., Department of Endocrinology, The Second Affiliated Hospital of Xiamen Medical College, Xiamen, China., Department of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

Abstract:  Despite the administration of exogenous insulin and other medications used to control many aspects of diabetes mellitus (DM), increased oxidative stress has been increasingly acknowledged in DM development and complications. Therefore, this study aims to investigate the role of advanced glycation end-products (AGEs) in oxidative stress (OS) of thyroid cells in patients with DM. Patients with DM with or without thyroid dysfunction (TD) were enrolled. Thyroid toxic damage was induced by adding AGE-modified bovine serum albumin (AGE-BSA) to normal human thyroid follicular epithelial cells. The cell viability, cell cycle, and cell apoptosis, as well as the content of reactive oxygen species (ROS), catalase (CAT), and malondialdehyde (MDA) in cells were measured. Thyroid hormones, T3, T4, FT3, and FT4 levels were measured by enzyme-linked immunosorbent assay. Receptor for advanced glycation end products (RAGE), sirtuin1 ( Sirt1), and NF-E2-related factor 2 ( Nrf2) expressions were detected, and the mitochondrial membrane potential was measured. We found increased AGEs in the serum of DM patients with TD. By increasing AGE-BSA concentration, cell viability; the thyroid hormones T3, T4, FT3, and FT4 levels; and mitochondrial membrane potential all significantly decreased. However, the increase in AGE-BSA concentration led to an increase in cell apoptosis, RAGE, and nuclear factor-Œ∫B expressions but produced the opposite effect on Sirt1, Nrf2, and heme oxygenase-1 expressions, as well as a decrease in antioxidant response element protein levels. The AGE-BSA increased ROS and MDA levels and reduced CAT level in normal human thyroid follicular epithelial cells on a dose independence basis. Our results demonstrated that AGEs-mediated direct increase of RAGE produced OS in thyroid cells of DM by inactivating the Sirt1/Nrf2 axis. 

Retracted: Yes

PubPeer comments:
 Fig 8C.  The determination by Western blot analysis demonstrated that ectopic expression of AGEs decreased the protein levels of Sirt1, Nrf2, ARE, and HOu20101, and increased the protein levels of RAGE and NFu2010u03baB.  The protein blobs come from a recognised oeuvre. For comparison: Figs 2B, 6B, 9B from [Shu et al (2018)] . Picking one example at random from [a spreadsheet] .  , 
 Fig 4C.  The DNA content of PIu2010stained cells at the G0 G1, S, and G2 M phases. B, The percentage of PIu2010stained cells at the G0 G1, S, and G2 M phases. C, Normal thyroid follicular epithelial cells in the scatter plots in which the upper left quadrant identified the necrotic cells (Annexin Vu2212 PI+), the upper right quadrant identified the late apoptotic cells (Annexin V+ PI+), the lower left quadrant identified the live cells (Annexin Vu2212 PIu2212), and the lower right quadrant identified the early apoptotic cells (Annexin V+ PIu2212).  Some panels (marked with colored rectangles) have similar counterparts in (inter alia) {fig 4A of [Zhou et al (2018)] ,  and Fig 8C in [An et all (2018)] ,  and Fig 13(a) of S[ong, Wang Huo (2019)] .  , 
 [Retracted 30 June 2021] . ----------------------- The above article, published online on 15 October 2018 in Wiley Online Library has been retracted by agreement between the authors, the journal s Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed after allegations had been raised by a third party. The authors stated that the experimental data in the article could not be reproduced, and thus, they consider the conclusions of this article to be invalid. ,