Sequential activation of different pathway networks in ischemia-affected and non-affected myocardium, inducing intrinsic remote conditioning to prevent left ventricular remodeling

Sci Rep. 2017 Mar 7:7:43958. doi: 10.1038/srep43958.

Abstract

We have analyzed the pathway networks of ischemia-affected and remote myocardial areas after repetitive ischemia/reperfusion (r-I/R) injury without ensuing myocardial infarction (MI) to elaborate a spatial- and chronologic model of cardioprotective gene networks to prevent left ventricular (LV) adverse remodeling. Domestic pigs underwent three cycles of 10/10 min r-I/R by percutaneous intracoronary balloon inflation/deflation in the mid left anterior descending artery, without consecutive MI. Sham interventions (n = 8) served as controls. Hearts were explanted at 5 h (n = 6) and 24 h (n = 6), and transcriptomic profiling of the distal (ischemia-affected) and proximal (non-affected) anterior myocardial regions were analyzed by next generation sequencing (NGS) and post-processing with signaling pathway impact and pathway network analyses. In ischemic region, r-I/R induced early activation of Ca-, adipocytokine and insulin signaling pathways with key regulator STAT3, which was also upregulated in the remote areas together with clusterin (CLU) and TNF-alpha. During the late phase of cardioprotection, antigen immunomodulatory pathways were activated with upregulation of STAT1 and CASP3 and downregulation of neprilysin in both zones, suggesting r-I/R induced intrinsic remote conditioning. The temporo-spatially differently activated pathways revealed a global myocardial response, and neprilysin and the STAT family as key regulators of intrinsic remote conditioning for prevention of adverse remodeling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Computational Biology
  • Disease Models, Animal
  • Gene Expression Profiling
  • Gene Regulatory Networks*
  • High-Throughput Nucleotide Sequencing
  • Ischemia / pathology*
  • Myocardial Reperfusion Injury / pathology*
  • Neprilysin / biosynthesis
  • Physical Conditioning, Animal / methods*
  • STAT1 Transcription Factor / biosynthesis
  • STAT3 Transcription Factor / biosynthesis
  • Signal Transduction*
  • Sus scrofa
  • Ventricular Remodeling*

Substances

  • STAT1 Transcription Factor
  • STAT3 Transcription Factor
  • Neprilysin