Targeted disruption of the heat shock protein 20–phosphodiesterase 4D (PDE4D) interaction protects against pathological cardiac remodelling in a mouse model of hypertrophy

Tamara Martin, Maria Hortigon-Vinagre, Jane Findlay, Christina Elliott, Susan Currie, George Baillie

Research output: Contribution to journalArticle

18 Citations (Scopus)
81 Downloads (Pure)

Abstract

Phosphorylated heat shock protein 20 (HSP20) is cardioprotective. Using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and a mouse model of pressure overload mediated hypertrophy, we show that peptide disruption of the HSP20–phosphodiesterase 4D (PDE4D) complex results in attenuation of action potential prolongation and protection against adverse cardiac remodelling. The later was evidenced by improved contractility, decreased heart weight to body weight ratio, and reduced interstitial and perivascular fibrosis. This study demonstrates that disruption of the specific HSP20–PDE4D interaction leads to attenuation of pathological cardiac remodelling.
Original languageEnglish
Pages (from-to)923-927
Number of pages5
JournalFEBS Open Bio
Volume4
Early online date28 Oct 2014
DOIs
Publication statusPublished - 2014

Keywords

  • cardiac remodeling
  • cardiac hypertrophy
  • peptide disruption

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