Open Access

Abnormal expression of miR‑133a in patients with acute myocardial infarction following radical surgery for gastric cancer and the underlying mechanism

  • Authors:
    • Jing Yu
    • Xufen Cao
    • Ye Zheng
    • Liqiu Yan
    • Jiawang Wang
  • View Affiliations

  • Published online on: October 10, 2018     https://doi.org/10.3892/mmr.2018.9541
  • Pages: 5023-5029
  • Copyright: © Yu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


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.
View Figures
View References

Related Articles

Journal Cover

December-2018
Volume 18 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Yu J, Cao X, Zheng Y, Yan L and Wang J: Abnormal expression of miR‑133a in patients with acute myocardial infarction following radical surgery for gastric cancer and the underlying mechanism. Mol Med Rep 18: 5023-5029, 2018
APA
Yu, J., Cao, X., Zheng, Y., Yan, L., & Wang, J. (2018). Abnormal expression of miR‑133a in patients with acute myocardial infarction following radical surgery for gastric cancer and the underlying mechanism. Molecular Medicine Reports, 18, 5023-5029. https://doi.org/10.3892/mmr.2018.9541
MLA
Yu, J., Cao, X., Zheng, Y., Yan, L., Wang, J."Abnormal expression of miR‑133a in patients with acute myocardial infarction following radical surgery for gastric cancer and the underlying mechanism". Molecular Medicine Reports 18.6 (2018): 5023-5029.
Chicago
Yu, J., Cao, X., Zheng, Y., Yan, L., Wang, J."Abnormal expression of miR‑133a in patients with acute myocardial infarction following radical surgery for gastric cancer and the underlying mechanism". Molecular Medicine Reports 18, no. 6 (2018): 5023-5029. https://doi.org/10.3892/mmr.2018.9541