Open Access

Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury

  • Authors:
    • Xian Long
    • Yongpan Huang
    • Jianbin He
    • Xiang Zhang
    • Yan Zhou
    • Yingmin Wei
    • Ying Tang
    • Lijing Liu
  • View Affiliations

  • Published online on: September 17, 2021     https://doi.org/10.3892/mmr.2021.12446
  • Article Number: 806
  • Copyright: © Long et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Septicemia is associated with excessive inflammation, oxidative stress and apoptosis, causing myocardial injury that results in high mortality and disability rates worldwide. The abnormal expression of multiple microRNAs (miRNAs/miRs) is associated with more severe sepsis‑induced myocardial injury (SIMI) and miR‑335 has been shown to protect cardiomyocytes from oxidative stress. The present study aimed to investigate the role of miR‑335 in SIMI. An SIMI model was established by cecal ligation and puncture (CLP) in mice. An miRNA‑335 precursor (pre‑miR‑335) was transfected to accelerate miR‑335 expression and an miR‑335 inhibitor (anti‑miR‑335) was used to inhibit miR‑335 expression. CLP or sham surgery was performed on pre‑miR‑335, anti‑miR‑335 and wild‑type mice and miR‑335 expression was determined by reverse transcription‑quantitative PCR. Inflammatory factors (TNF‑α, IL‑6 and IL‑10) and troponin (cTNI), brain natriuretic peptide (BNP), creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) were assessed using commercial kits. Apoptosis was detected by flow cytometry and cardiac function was assessed using a Langendorff isolated cardiac perfusion system. miR‑335 expression was upregulated and an elevation in inflammatory factors and cTNI, BNP, CK, LDH and AST was observed. Compared with the wild‑type control group, pre‑miR‑335 mice treated with CLP exhibited significantly reduced left ventricular development pressure, maximum pressure increased reduction rates, as well as decreased levels of TNF‑α, IL‑6 and IL‑10, myocardial injury and apoptosis; by contrast, these features were amplified in CLP‑treated anti‑miR‑335 mice. In conclusion, the upregulation of miR‑335 exerted ameliorative effects on myocardial injury following sepsis and may indicate a novel therapeutic intervention for SIMI.
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November-2021
Volume 24 Issue 5

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Copy and paste a formatted citation
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Spandidos Publications style
Long X, Huang Y, He J, Zhang X, Zhou Y, Wei Y, Tang Y and Liu L: Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury. Mol Med Rep 24: 806, 2021.
APA
Long, X., Huang, Y., He, J., Zhang, X., Zhou, Y., Wei, Y. ... Liu, L. (2021). Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury. Molecular Medicine Reports, 24, 806. https://doi.org/10.3892/mmr.2021.12446
MLA
Long, X., Huang, Y., He, J., Zhang, X., Zhou, Y., Wei, Y., Tang, Y., Liu, L."Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury". Molecular Medicine Reports 24.5 (2021): 806.
Chicago
Long, X., Huang, Y., He, J., Zhang, X., Zhou, Y., Wei, Y., Tang, Y., Liu, L."Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury". Molecular Medicine Reports 24, no. 5 (2021): 806. https://doi.org/10.3892/mmr.2021.12446