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Vitexin protects isoproterenol induced post myocardial injury by modulating hipposignaling and ER stress responses

Rathinavel Ashokkumar1, Sankar Jamuna1, M S Sakeena Sadullah1

  • 1Department of Biochemistry, University of Madras, Guindy Campus, Chennai 600 025, India.

Biochemical and Biophysical Research Communications
|February 7, 2018
PubMed

Insights

This study reveals how endoplasmic reticulum (ER) stress causes heart muscle cell death after myocardial infarction. The bioflavonoid Vitexin effectively protects the heart by inhibiting ER stress and related signaling pathways.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Endoplasmic reticulum (ER) stress plays a role in myocardial injury, but its precise molecular mechanisms are not fully understood.
  • Investigating ER stress-mediated myocyte death is crucial for developing effective therapeutic strategies for myocardial infarction.

Purpose of the Study:

  • To elucidate the molecular mechanisms of ER stress-induced myocyte death in Isoproterenol (ISO)-induced myocardial infarction (MI).
  • To evaluate the cardioprotective effects of Vitexin, a bioflavonoid, against ISO-induced myocardial injury.

Main Methods:

  • Myocardial infarction was induced using Isoproterenol (ISO).
  • Assessed ER permeabilization, reactive oxygen species (ROS) production, caspase-3 activation, Bcl2 family protein modulation, and bnip3 activation.
  • Investigated the effect of Vitexin on ISO-induced translocation of C/EBP homologous protein (CHOP) to the nucleus.
  • Examined the modulation of Mst1 (a kinase) and Hippo signaling pathway components (p-Yap, p-Mst1) by Vitexin.

Main Results:

  • ISO-induced apoptosis was linked to ER permeabilization, increased ROS, caspase-3 activation, altered Bcl2 proteins, and bnip3 activation.
  • Vitexin treatment inhibited ISO-induced CHOP nuclear translocation and Mst1 activation.
  • Vitexin significantly reduced the expression of phosphorylated Yes-associated protein (p-Yap) and phosphorylated Mst1 (p-Mst1) elevated during post-MI.

Conclusions:

  • ISO triggers myocardial injury through coordinated activation of ER stress and the Hippo signaling pathway.
  • Vitexin exhibits potent cardioprotective effects by ameliorating ER stress and inhibiting the Hippo signaling pathway during myocardial infarction.
Keywords:
ApoptosisER stressHippo signalingPost MIUPRVitexin

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