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SENP3 protects H9C2 cells from apoptosis triggered by H/R via STAT3 pathway

Y Zhang1, L-M Zheng, C-X Wang

  • 1Departments of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China. renjixuesong@163.com.

European Review for Medical and Pharmacological Sciences
|May 18, 2018
PubMed
Abstract

Insights

SENP3 protects H9C2 cells from heart/reperfusion injury by activating the JAK2/STAT3 pathway. This protein reduces apoptosis and reactive oxygen species, offering a potential therapeutic target for myocardial ischemia-reperfusion injury.

Area of Science:

  • Cardiovascular Biology
  • Cellular Stress Response
  • Molecular Signaling

Background:

  • Myocardial ischemia-reperfusion (I/R) injury is a major cause of heart damage.
  • H9C2 cardiomyoblasts are a widely used cell model for studying cardiac I/R injury.
  • The role of SENP3 in protecting against I/R injury via the STAT3 pathway requires further elucidation.

Purpose of the Study:

  • To investigate the protective role of SENP3 against H9C2 cell apoptosis induced by H/R.
  • To determine if this protection is mediated through the signal transducer and activator of transcription 3 (STAT3) pathway.

Main Methods:

  • Established mouse models of myocardial I/R and cultured H9C2 cells.
  • Quantified reactive oxygen species (ROS) using DCFH assay.
  • Assessed apoptosis via flow cytometry and detected protein/gene expression (p-JAK2, JAK2, STAT3, p-STAT3, c-caspase3, Bcl/Bax) using Western blotting and RT-PCR.

Main Results:

  • SENP3 and p-STAT3 levels increased in I/R mice and H9C2 cells post-H/R.
  • SENP3 accumulation was ROS-dependent and inhibited by N-acetylcysteine (NAC).
  • SENP3 inhibition promoted apoptosis and c-caspase3 expression, while SENP3 overexpression reduced apoptosis.

Conclusions:

  • SENP3 protects H9C2 cells from H/R-induced apoptosis.
  • This protective effect is achieved by enhancing the JAK2/STAT3 signaling pathway.

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