Retracted : Emodin protects H9c2 cells against hypoxia‐induced injury via regulation of miR‐26a/survivin and the JAK1/STAT3 pathway
Authors: Jun Wang
Xiaobing Li
Pujuan Liu
Jiancheng Huang
Hongying Li
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Congenital heart disease (CHD); JNK/STAT3; emodin; miR-26a; survivin.
Affiliations: Department of Congenital Heart Disease, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.

Abstract:  Background/aim: Congenital heart disease (CHD) is a catastrophic disease. Emodin possesses biological properties in protecting against some diseases. Our study investigated to explore the effects of emodin on hypoxia-stimulated cardiomyocytes, which mimicked CHD in vitro. Methods: H9c2 cells were stimulated with hypoxia and then the cells were treated with or without emodin, and/or transfected with miR-26a mimic, pcDNA-survivin and their corresponding negative control (NC). Cell viability and cell apoptosis were detected by Cell Counting kit-8 assay and flow cytometry, respectively. In addition, the expression of apoptotic proteins, Janus kinase 1 (JNK)/signal transducer and activator of transcription 3 (STAT3) pathway factors, and survivin were evaluated by using Western blot analysis. The expression of miR-26a was analyzed by quantitative real time polymerase chain reaction (qRT-PCR). Moreover, the target of miR-26a was verified by using a luciferase report assay. Results: Hypoxia significantly decreased cell viability and increased cell apoptosis, and the accumulated levels of cleaved caspase-3 and cleaved-caspase-9 were upregulated by hypoxia compared with the control. However, emodin administration led to the opposite result. A further result showed that emodin increased the phosphorylation of JNK/STAT3 pathway-related proteins and the pathway inhibitor AG490 impaired the protective effects of emodin on hypoxia-induced injury. In addition, emodin negatively regulated the miR-26a expression, and overexpression of miR-26a enhanced cell apoptosis and upregulated the expression of cleaved-caspase-3 and cleaved-caspase-9 compared with the NC. Moreover, emodin statistically upregulated the expression of survivin, and overexpression of miR-26a decreased the expression of survivin. The luciferase of miR-26a overexpression was decreased in the wild type of the survivin group. Conclusion: Emodin protects hypoxia-induced cell injury as evidenced by increasing cell viability and decreasing apoptosis through downregulation of miR-26a as well as activation of the JNK/STAT3 pathway. 

Retracted: Yes

PubPeer comments:
 This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels. Despite these similarities, these papers are authored by researchers from different departments and institutes, with almost no overlap in authors. The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing A more detailed description of this set of papers, suspected to all be generated by a common source, a paper mill , can be found here: * https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers (January 2020) * https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill (February 2020) The same paper mill has been described in these papers: * Jana Christopher - Systematic fabrication of scientific images revealed - FEBS Letters (2018) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13201 * Jennifer A Byrne and Jana Christopher - Digital magic, or the dark arts of the 21st centuryu2014how can journals and peer reviewers detect manuscripts and publications from paper mills? - FEBS Letters (2020) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13747 , 
 Retracted [8 June 2021] . -------------------------------------------------- The above article, published online on 30 January 2019 in Wiley Online Library , has been retracted by agreement between the journal s Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. The authors collaborated in the investigation initially, but were not available for a final confirmation of the retraction. ,