CIRBP protects H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway
Authors: F Kuang
R Jing
Z X Qian
T L Yang
L Huang
T Y Long
Journal: Brazilian Journal of Medical and Biological Research (2017)
Discipline: CLINICAL MEDICINE
Keywords: Myocardial ischemia; Cold inducible RNA-binding protein (CIRBP); Cell proliferation; Cell apoptosis; Reactive oxygen species (ROS)
Affiliations: Cardiovascular Department, The Xiangya Hospital of Central South University, Changsha City, Hunan Province, China., Department of Cardiac Surgery, The First Affiliated Hospital of Xiamen University, Xiamen City, Fujian Province, China., Department of Cardiac Surgery, Shenzhen Hospital of Peking University, Shenzhen City, Guangdong Province, China., Department of Emergency, The Xiangya Hospital of Central South University, Changsha City, Hunan Province, China.

Abstract:  Myocardial ischemia is a major cause of death and remains a disease with extremely deficient clinical therapies and a major problem worldwide. Cold inducible RNA-binding protein (CIRBP) is reported to be involved in multiple pathological processes, including myocardial ischemia. However, the molecular mechanisms of myocardial ischemia remain elusive. Here, we first overexpressed CIRBP by transfection of pc-CIRBP (pcDNA3.1 containing coding sequenced for CIRBP) and silenced CIRBP by transfection of small interfering RNA targeting CIRBP (siCIRBP). pcDNA3.1 and the negative control of siCIRBP (siNC) were transfected into H9C2 cells to act as controls. We then constructed a cell model of myocardial ischemia through culturing cells in serum-free medium with hypoxia in H9C2 cells. Subsequently, AlamarBlue assay, flow cytometry and western blot analysis were used, respectively, to assess cell viability, reactive oxygen species (ROS) level and apoptosis, and expression levels of IκBα, p65 and Bcl-3. We demonstrated that CIRBP overexpression promoted cell proliferation (P&lt;0.001), inhibited cell apoptosis (P&lt;0.05), reduced ROS level (P&lt;0.001), down-regulated phosphorylated levels of IκBα and p65 (P&lt;0.01 or P&lt;0.001), and up-regulated expression of Bcl-3 (P&lt;0.001) in H9C2 cells with myocardial ischemia. The influence of CIRBP knockdown yielded opposite results. Our study revealed that CIRBP could protect H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway. 

Retracted: No

PubPeer comments:
 If I may quote from posts by Dr Elisabeth Bik: This paper belongs to a set of over 400 papers (as per May 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. ![file] ![file] 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 ,