Influence of miR-34a on myocardial apoptosis in rats with acute myocardial infarction through the ERK1/2 pathway
Authors: F-H Tian
L-H Jiang
S-X Wu
Y-F Sun
W-S Bian
Z-X Kang
Z Zhuo
B-F Gao
X-Z Zhang
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-34a; myocardial apoptosis; ERK1/2 pathway; Sprague-Dawley rats; acute myocardial infarction
Affiliations: Department of Cardiovascular Medicine, Linyi No. 3 People's Hospital, Linyi, China. .

Abstract:  Objective: To study the influence of micro-ribonucleic acid (miR)-34a on myocardial apoptosis in rats with acute myocardial infarction (AMI) through the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway. Materials and methods: A total of 24 Sprague-Dawley (SD) rats were randomly divided into sham group (n=12) and model group (n=12). The heart was exposed in the sham group, while the AMI model was established in the model group. After sampling, the morphology of myocardial tissues was observed via hematoxylin-eosin (HE) staining, the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were detected via immunohistochemistry, and the protein expression levels of ERK1/2 and phosphorylated ERK1/2 (p-ERK1/2) were detected via Western blotting. Moreover, the expression of miR-34a was detected via quantitative Polymerase Chain Reaction (qPCR), the apoptosis was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the myocardial injury indexes were detected using a fully-automatic biochemical analyzer. Results: The morphology of myocardial tissues was normal with a complete structure in the sham group, while there was damage to myocardial tissues in different degrees in the model group. The immunohistochemical results revealed that the Bax expression was increased and the Bcl-2 expression was decreased in the model group compared with those in the sham group (p&lt;0.05). The results of Western blotting showed that the protein expression levels of both ERK1/2 and p-ERK1/2 were significantly increased in the model group compared with those in the sham group (p&lt;0.05). The qPCR results manifested that the expression of miR-34a in the model group markedly declined compared with that in the sham group (p&lt;0.05). Besides, the TUNEL detection showed that the apoptosis rate in the model group was remarkably increased compared with that in the sham group (p&lt;0.05), and the content of cardiac troponin T and creatine kinase isoenzyme in the model group was significantly higher than that in the sham group ((p&lt;0.05). Conclusions: MiR-34a affects the apoptosis in AMI by regulating the ERK1/2 signaling pathway. 

Retracted: No

PubPeer comments:
  Figure 1. Morphology of heart tissues observed via HE staining . Beneath, for comparison, Fig 2 from [Zhang et al (2020)] ,  Pathological injuries in rat heart tissues .  There are modifications, but the  Model panels are surprisingly similar for unrelated experiments from different teams at different institutions.  , 
 Fig 1 again,  Morphology of heart tissues observed via HE staining .  Sham and Model panels overlap with Sham and Butlphthalide panels within work by other authors. Figure 1.  Morphology of heart tissues via HE staining from [Bai et al (2019)] :  , 
 Figure 2.  Immunohistochemical detection of Bax and Bcl-2 expressions .  One panel also appears (labeled as Bax rather than Bcl-2) in work by other authors. Fig 3 from [Pan et al (2019)] :  Immunohistochemical detection .  ,