1. Academic Validation
  2. MicroRNA-30e protects the heart against ischemia and reperfusion injury through autophagy and the Notch1/Hes1/Akt signaling pathway

MicroRNA-30e protects the heart against ischemia and reperfusion injury through autophagy and the Notch1/Hes1/Akt signaling pathway

  • Int J Mol Med. 2018 Jun;41(6):3221-3230. doi: 10.3892/ijmm.2018.3548.
Jianjie Zheng 1 Jing Li 1 Bo Kou 1 Qiuyue Yi 1 Tao Shi 1
Affiliations

Affiliation

  • 1 Department of Cardiovascular Surgery, The First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.
Abstract

The aim of the present study was to determine the cardioprotective mechanisms by which micro (mi)RNA-30e protects the heart from myocardial ischemia/reperfusion injury (MI/R) and to explore the signaling pathways that may confer protection for the heart and be potential therapeutic targets. It was demonstrated that miRNA‑30e expression was decreased in patients with MI/R. In H9C2 cells, silencing (si)miRNA‑30e significantly inhibited cellular Apoptosis, the expression of Apoptosis regulator Bax (Bax) and caspase‑3 activity. It also significantly increased the expression of microtubule‑associated proteins 1A/1B LIGHT chain 3B, p62, Beclin‑1, neurogenic locus Notch homolog protein‑1 (Notch1), Hes1 and phosphorylated‑protein kinase B (p‑Akt), and decreased the expression of inducible NO Synthase (iNOS) and proteins associated with oxidative stress. The inhibition of Autophagy following treatment with 3‑methyladenine significantly reversed the effect of si‑miRNA‑30e on Apoptosis, Bax, caspase‑3, iNOS and oxidative stress in H9C2 cells. The promotion of Notch1 expression increased the effect of si‑miRNA‑30e on Apoptosis, Bax, caspase‑3, iNOS, Notch1, Hes1 and p‑Akt protein expression and oxidative stress in H9C2 cells. Taken together, these results indicate that miRNA‑30e protects the heart from MI/R via Autophagy and the Notch1/Hes1/Akt signaling pathway.

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