Ji-Ning Jia1,2,3,4†Xi-Xi Yin5†Qin Li1,2,3,4Qi-Wen Guan1,2,3,4Nan Yang1,2,3,4Kang-Ni Chen1,2,3,4
Hong-Hao Zhou1,2,3,4
Xiao-Yuan Mao1,2,3,4*- 1Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, China
- 2Institute of Clinical Pharmacology, Central South University, Hunan Key Laboratory of Pharmacogenetics, Changsha, China
- 3Engineering Research Center of Applied Technology of Pharmacogenomics, Ministry of Education, Changsha, China
- 4National Clinical Research Center for Geriatric Disorders, Changsha, China
- 5Department of Pediatrics, Xiangya Hospital, Central South University, Changsha, China
A Corrigendum on
Neuroprotective Effects of the Anti-cancer Drug Lapatinib Against Epileptic Seizures via Suppressing Glutathione peroxidase 4-Dependent Ferroptosis
by Jia, J.-N., Yin, X.-X., Li, Q., Guan, Q.-W., Yang, N., Chen, K.-N., Zhou, H.-H., and Mao, X.-Y. (2020). Front. Pharmacol. 11:601572. doi: 10.3389/fphar.2020.601572
In the original article, there was a mistake in Figure 5F and Figure 6B as published. Due to our carelessness in the process of rearranging these figures, the image in the “Era + Fer-1” group within Figure 5F and the image in the “Lap” group within Figure 6B were uploaded with mistakes. The corrected Figure 5 and Figure 6 appears below.
FIGURE 5. Lapatinib prevents Glu- or erastin-induced neuronal death possibly by suppressing ferroptosis (A–D) Detection of lipid ROS, 4-HNE and MDA content in the glutamate (Glu)- or erastin (Era)-induced HT22 cell death model following lapatinib (Lap) (10 μM) and ferrostatin-1 (Fer-1) (12.5 μM) pretreatment for 2 h (E) RT-qPCR analysis of PTGS2 mRNA expression pretreated with or without Lap (10 μM) and Fer-1 (12.5 μM) in HT22 cells induced by Glu or Era (F,G) Comparisons of combination of Lap and ferroptosis inhibitors and Lap alone in HT22 cells following Glu or Era challenge when pretreatment with Lap (10 μM), Fer-1 (12.5 μM), liproxstatin-1 (Lip-1) (1 μM) and deferoxamine (DFO) (50 μM) pretreatment for 2 h. Scale bar: 200 μm. All results were presented as the mean ± SEM from three independent experiments, ns indicates no statistical significance. **p < 0.01 and ***p < 0.001.
FIGURE 6. Lapatinib inhibits neuronal ferroptosis by blocking the downregulation of GPX4 (A) Effects of lapatinib (Lap) or ferrostatin-1 (Fer-1) on the expressions of ferroptosis-related proteins including glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), 5-Lipoxygenase (5-LOX) or acyl-CoA synthetase 4 (ACSL4) in HT22 cell death model induced by glutamate (Glu) or erastin (Era). The value below the band is obtained via ImageJ analysis (B) Immunofluorescence analysis of GPX4 expression after pretreatment for 2 h with Lap (10 μM), followed by exposure to Glu or Era for another 8 h in HT22 cells. Scale bar: 50 μm (C) GSH level was assessed following Lap (10 μM) pretreatment for 2 h (D,E) Effects of GPX4 inhibition by ras-selective lethal small molecule 3 (RSL3) (1 nM) on the neuroprotection of Lap (10 μM) against Glu- or erastin-induced cell death in HT22 cells. Scale bar: 200 μm. All results were shown as the mean ± SEM from three independent experiments, ns means the difference is not statistically significant, ***p < 0.001.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: lapatinib, epileptic seizures, neuroprotection, ferroptosis, lipid peroxidation, glutathione peroxidase 4
Citation: Jia J-N, Yin X-X, Li Q, Guan Q-W, Yang N, Chen K-N, Zhou H-H and Mao X-Y (2022) Corrigendum: Neuroprotective Effects of the Anti-Cancer Drug Lapatinib Against Epileptic Seizures via Suppressing Glutathione Peroxidase 4-Dependent Ferroptosis. Front. Pharmacol. 12:810295. doi: 10.3389/fphar.2021.810295
Received: 06 November 2021; Accepted: 17 November 2021;
Published: 03 January 2022.
Edited and reviewed by:
Ashok Kumar, University of Florida, United StatesCopyright © 2022 Jia, Yin, Li, Guan, Yang, Chen, Zhou and Mao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Xiao-Yuan Mao, maoxiaoyuan2011@163.com
†These authors have contributed equally to this work