miR-26a prevents neural stem cells from apoptosis via Œ≤-catenin signaling pathway in cardiac arrest-induced brain damage
Authors: Fang Li
Xiaoxing Liao
Jie Zhang
Hengjie Li
Yubin Deng
Xin Li
Chunlin Hu
Hongyan Wei
Journal: Bioscience Reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: GSK-3Œ≤; NSCs and CA; miR-26a; Œ≤-catenin.
Affiliations: Department of Emergency, the Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, China, Department of Emergency, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China, The Second Department of Hepatobiliary Surgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650032, China, Translational Medicine Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China

Abstract:  Neural stem cells (NSCs) transplantation is one of the most promising strategies for the treatment of CA-induced brain damage. The transplanted NSCs could differentiate into new neuron and replace the damaged one. However, the poor survival of NSCs in severe hypoxic condition is the limiting step to make the best use of this kind of therapy. In the present study, we investigated whether the overexpression of miR-26a improves the survival of NSCs in hypoxic environment in vitro and in vivo. In vitro hypoxia injury model is established in NSCs by CoCl2 treatment, and in vivo cardiac arrest (CA) model is established in Sprague-Dawley (SD) rats. Quantitative real-time polymerase chain reaction is used to detect the mRNA level and Western blot is used to examine the protein level of indicated genes. TUNEL staining and flow cytometry are applied to evaluate apoptosis. Dual-luciferase reporter assay is utilized to analyze the target gene of miR-26a. The expression of miR-26a is reduced in both in vitro and in vivo hypoxic model. MiR-26a directly targets 3'-UTR of glycogen synthase kinase 3Œ≤ (GSK-3Œ≤), resulting in increased Œ≤-catenin expression and decreased apoptosis of NSCs. Overexpression of miR-26a in transplanted NSCs improves the survival of NSCs and neurological function in CA rats. MiR-26a prevents NSCs from apoptosis by activating Œ≤-catenin signaling pathway in CA-induced brain damage model. Modulating miR-26a expression could be a potential strategy to attenuate brain damage induced by CA. 

Retracted: No

PubPeer comments:
  , 
 #1 Brightness contrast adjusted  , 
 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. , 
 #1 Thanks for your comments. We just saw the expression of concern and pubpeer comments recently. We have checked the manuscript and original data carefully and provided the original pictures to the editorial office. Thank you very much! , 
 #1 Thanks for your comments. We just saw the expression of concern and pubpeer comments recently. We have checked the manuscript and original data carefully. We have provided the original pictures to the editorial office. Thank you very much! , 
 #5 Thank you for responding. Could the authors also post here the original uncropped scans used to generate Figure 4A? Can the authors also provide institutional email addresses? These seem similar to those used by u201cpaper mills.u201d Correspondence: Xiaoxing Liao (nhfxg97@163.com) or Yubin Deng (jxrfia2@163.com) ***  , 
 Retracted [4 May 2021](10.1042 BSR-20181635_RET). ------------------------------------ This Retraction follows an Expression of Concern relating to this article previously published by Portland Press. This article is being retracted from Bioscience Reports at the request of the authors following receipt of a notification from a reader, alerting the authors to a row of duplicated images with differing contrasts in Figure 2A. The authors are unable to correct the article and wish to retract the article. The Editor-in-Chief and Editorial Board agree with the retraction. ,