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In Vitro Analysis of E3 Ubiquitin Ligase Function
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In Vitro Analysis of E3 Ubiquitin Ligase Function

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E3 ligase Fbw7 participates in oxidative stress‑induced myocardial cell injury via interacting with Mcl‑1

Xia Li1, Naijin Zhang1, Ying Zhang2

  • 1Department of Cardiovascular Medicine, First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.

Molecular Medicine Reports
|July 2, 2019
PubMed

Insights

Oxidative stress causes heart disease. Researchers found F-box and WD repeat domain containing 7 (Fbw7) may degrade Mcl-1, promoting heart cell injury via the Mcl-1-Bax pathway.

Area of Science:

  • Biochemistry
  • Cardiovascular Biology
  • Cellular Biology

Background:

  • Oxidative stress is a key factor in myocardial cell injury and heart diseases.
  • Ubiquitylation is increasingly recognized for its role in apoptosis.
  • Understanding the interplay of E3 ligases and apoptosis regulators is crucial for cardiovascular research.

Purpose of the Study:

  • To investigate the interaction between F-box and WD repeat domain containing 7 (Fbw7) and MCL1 apoptosis regulator (Mcl-1) in myocardial cells under oxidative stress.
  • To elucidate the role of Fbw7 and Mcl-1 in the apoptosis pathway during oxidative stress-induced myocardial injury.

Main Methods:

  • Cell Counting Kit-8 assay for cell viability.
  • Flow cytometry for apoptosis analysis.
  • Western blot and co-immunoprecipitation assays to study protein interactions and degradation.
  • Reactive oxygen species assays to quantify oxidative stress.

Main Results:

  • Fbw7 was found to potentially facilitate apoptosis through the Mcl-1-Bax pathway in H9c2 cells experiencing oxidative stress.
  • Fbw7 appears to degrade Mcl-1, thereby impairing Mcl-1's function in maintaining cell viability.
  • Evidence suggests Fbw7's interaction with Mcl-1 promotes myocardial cell injury.

Conclusions:

  • Fbw7 plays a significant role in promoting myocardial cell injury during oxidative stress.
  • The Fbw7-mediated degradation of Mcl-1 is a potential mechanism contributing to apoptosis in oxidative stress conditions.
  • Targeting the Fbw7-Mcl-1 interaction could offer therapeutic strategies for heart diseases associated with oxidative stress.

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