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MiR-410 inhibition induces HUVECs proliferation and represses ox-LDL-triggered apoptosis through activating STAT3

Ming-Yan Hu1, Xiong-Bing Du1, Hai-Bo Hu2

  • 1Department of Cardiology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|March 9, 2018
PubMed

Insights

MicroRNA-410 (miR-410) promotes atherosclerosis by impairing endothelial cell function. Silencing miR-410 protects against ox-LDL-induced injury by activating STAT3, offering a potential therapeutic target for atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cell Biology

Background:

  • Oxidized low-density lipoprotein (ox-LDL) is implicated in endothelial cell injury and atherosclerosis (AS) development.
  • MicroRNAs (miRNAs) are key regulators in various diseases, including AS, by modulating gene expression.
  • The specific role of miR-410 in ox-LDL-induced endothelial dysfunction requires elucidation.

Purpose of the Study:

  • To investigate the underlying mechanism of miR-410 in ox-LDL-induced endothelial cell injury and its relevance to atherosclerosis.
  • To determine the effect of miR-410 modulation on human umbilical vein endothelial cells (HUVECs) exposed to ox-LDL.
  • To identify the molecular targets and pathways regulated by miR-410 in the context of AS.

Main Methods:

  • Assessed the impact of ox-LDL on HUVEC proliferation and apoptosis.
  • Quantified miR-410 expression levels in ox-LDL-treated HUVECs.
  • Utilized miR-410 knockdown and signal transducer and activator of transcription 3 (STAT3) overexpression in HUVECs.
  • Validated the interaction between miR-410 and STAT3 using a dual-luciferase assay.

Main Results:

  • Ox-LDL inhibited HUVEC growth and induced apoptosis in a dose- and time-dependent manner.
  • miR-410 expression was significantly upregulated in ox-LDL-treated HUVECs.
  • miR-410 knockdown promoted HUVEC proliferation and alleviated ox-LDL-induced apoptosis.
  • STAT3 expression was decreased by ox-LDL, and STAT3 was identified as a direct target of miR-410.
  • STAT3 overexpression rescued ox-LDL-induced AS-related cellular events.

Conclusions:

  • miR-410 plays a critical role in ox-LDL-induced endothelial cell injury, contributing to atherosclerosis.
  • Silencing miR-410 inhibits ox-LDL-induced HUVEC proliferation and apoptosis by activating the STAT3 pathway.
  • Targeting miR-410 represents a potential therapeutic strategy for mitigating ox-LDL-induced endothelial dysfunction and AS progression.
Keywords:
AtherosclerosisHUVECsSTAT3miR-410ox-LDL

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