The targeted regulation of miR-26a on PTEN-PI3K/AKT signaling pathway in myocardial fibrosis after myocardial infarction
Authors: R Cui
S Zhang
Journal: European Review for Medical and Pharmacological Sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: MiR-26a; myocardial fibrosis; PTEN; PI3K/AKT signaling pathway; MMP-9
Affiliations: Department of Cardiology, Heilongjiang provincial Hospital,Harbin, Heilongjiang, P.R. China. .

Abstract:  Objective: MiR-26a is involved in regulating myocardial remodeling and it is also related to organ fibrosis. Its role in myocardial fibrosis process is still controversy. As a definite target gene of miR-26a, phosphatase and tensin homology does on chromosome ten (PTEN) plays a role in regulating PTEN-PI3K/AKT signaling pathway. This study explored the function of miR-26a in regulating PTEN-PI3K/AKT signaling pathway, MMP-9 expression, and myocardial fibrosis after acute myocardial infarction (AMI). Materials and methods: AMI model was established on Sprague-Dawley (SD) rats. Hydroxyproline, COL1A1, miR-26a, PTEN, p-AKT, and MMP-9 expressions in myocardial tissue at 1 week, 2 weeks, and 4 weeks after modeling were detected. Human cardiac fibroblasts (HCF) were cultured in vitro to detect miR-26a, PTEN, p-AKT, MMP-9, COL1A1, and Œ±-SMA expressions in the process of myofibroblast differentiation (P1, P3, P5). HCF in P5 were transfected with miR-26a mimics or inhibitor to test miR-26a, PTEN, p-AKT, MMP-9, COL1A1, and Œ±-SMA expressions. Results: Hydroxyproline, COL1A1, miR-26a, p-AKT, and MMP-9 overexpressed, while PTEN downregulated in myocardial tissue during the process of myocardial fibrosis after AMI. MiR-26a, PTEN, p-AKT, MMP-9, COL1A1, and Œ±-SMA expression gradually enhanced, while PTEN declined, following the process of HCF differentiating into myofibroblast. MiR-26a elevation suppressed PTEN expression, and increased p-AKT, MMP-9, COL1A1, and Œ±-SMA levels. MiR-26a reduction significantly upregulated PTEN level, weakened PI3K/AKT signaling pathway activity, and declined MMP-9, COL1A1, and Œ±-SMA protein expression. Conclusions: MiR-26a upregulation may play a role in myocardial fibrosis after AMI by suppressing PTEN, enhancing PI3K/AKT signaling pathway and MMP-9 levels. 

Retracted: Yes

PubPeer comments:
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 #2 I agree that these donu2019t appear to be definitively problematic. I *can* see some sharpish background transitions in 4A (inverse below) but may just be compression artifacts. Higher quality scans of original blots might address any concerns quickly. ***  , 
 2020 retraction. https: www.ncbi.nlm.nih.gov pubmed 32103388 The Editors-in-Chief have retracted this article [1] following an investigation by the University of Maryland. The institution found that in Figure 1C, the graph showing PDGF-B does not match the original data for the 24-hour time point. The graph shows the value to be over 1000 pg ml, but the original data have a value of 106.626. In Figure 1F, the data were entered manually to create the standard deviation bars. The data manually entered do not match the original data. When the standard deviations for the original data were calculated, the p values were no longer significant using a paired student t test. In Figure 2C, the original data do not match the published data. In Figure 4B, the images in the first lane and the fifth lane are from the same micrograph (i.e., the same set of conditions). However, the published figure claims that they are different conditions. The metadata in this figure also shows different cell lines than those noted in the article. The first and last images are labelled as  Du145 shAR3 anti AR3.jpg . The second image is labelled as  Du145 shAR8 anti AR8.jpg . The third image is labelled as  Cos1 mARs3 mS3-2 antibody-2.jpg. The fourth image is labelled as  R1 3634 bleed.jpg . Due to these errors, the Editors-in-Chief have found that the results are no longer reliable. , 
 https: retractionwatch.com 2020 03 03 four-retractions-follow-misconduct-inquiry-at-u-maryland ,