ArticleMolecular medicine reports2018
Abnormal expression of miR‑133a in patients with acute myocardial infarction following radical surgery for gastric cancer and the underlying mechanism.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- MicroRNA (miRNA): A New Dimension in the Pathogenesis of Antiphospholipid Syndrome (APS).International journal of molecular sciences · 2020Review
- Silence of miR-32-5p promotes endothelial cell viability by targeting KLF2 and serves as a diagnostic biomarker of acute myocardial infarction.Diagnostic pathology · 2020Article
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Authors and funding
5 authors.
Funding
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Abstract
The present study aimed to investigate the expression of microRNA (miR)‑133a in patients with or without acute myocardial infarction (AMI) following radical surgery for gastric cancer, and to explore its underlying mechanisms. Blood samples were collected from patients with or without AMI in order to detect the expression levels of miR‑133a and endothelial injury markers. In addition, an AMI rat model was established. Reverse transcription‑quantitative polymerase chain reaction was used to detect the mRNA expression levels of miR‑133a and B‑cell lymphoma 2‑like 1 (Bcl2l1). In addition, an ELISA assay was used for endothelial injury marker analysis. To investigate the effects of miR‑133a on human umbilical vein endothelial cells (HUVECs), a miR‑133a inhibitor was used. Cell proliferation and apoptosis were subsequently detected using an MTT assay and flow cytometry. Western blot analysis was also conducted to detect Bcl2l1 protein expression. The results suggested that patients with AMI exhibited significantly increased expression of endothelial injury markers (von Willebrand factor, heart‑type fatty acid‑binding protein and cardiac troponin I) and miR‑133a in blood samples compared with patients without AMI. In addition, treatment with a miR‑133a mimic was able to upregulate the expression of endothelial injury markers in an AMI rat model, whereas treatment with a miR‑133a inhibitor had the opposite effect. Furthermore, cellular experiments indicated that a miR‑133a inhibitor could promote HUVEC proliferation and reduce cell apoptosis. The present results also confirmed that miR‑133a directly targets Bcl2l1 and negatively regulates Bcl2l1 expression. In conclusion, the results of the present study suggested that miR‑133a was involved in the endothelial injury process after AMI by targeting Bcl2l1.
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