The Formin, DIAPH1, is a Key Modulator of Myocardial Ischemia/Reperfusion Injury

  1. O'Shea, Karen M. 1
  2. Ananthakrishnan, Radha 1
  3. Li, Qing 1
  4. Quadri, Nosirudeen 1
  5. Thiagarajan, Devi 1
  6. Sreejit, Gopalkrishna 1
  7. Wang, Lingjie 1
  8. Zirpoli, Hylde 1
  9. Aranda, Juan Francisco 1
  10. Alberts, Arthur S. 2
  11. Schmidt, Ann Marie 1
  12. Ramasamy, Ravichandran 1
  1. 1 a Diabetes Research Program, Department of Medicine, New York University Langone Medical Center, New York, NY 10016, USA
  2. 2 Center for Cancer and Cell Biology, Van Andel Research Institute, Grand Rapids, MI 49503, USA
Revista:
EBioMedicine

ISSN: 2352-3964

Año de publicación: 2017

Volumen: 26

Páginas: 165-174

Tipo: Artículo

DOI: 10.1016/J.EBIOM.2017.11.012 GOOGLE SCHOLAR lock_openAcceso abierto editor

Otras publicaciones en: EBioMedicine

Resumen

The biochemical, ionic, and signaling changes that occur within cardiomyocytes subjected to ischemia are exacerbated by reperfusion; however, the precise mechanisms mediating myocardial ischemia/reperfusion (I/R) injury have not been fully elucidated. The receptor for advanced glycation end-products (RAGE) regulates the cellular response to cardiac tissue damage in I/R, an effect potentially mediated by the binding of the RAGE cytoplasmic domain to the diaphanous-related formin, DIAPH1. The aim of this study was to investigate the role of DIAPH1 in the physiological response to experimental myocardial I/R in mice. After subjecting wild-type mice to experimental I/R, myocardial DIAPH1 expression was increased, an effect that was echoed following hypoxia/reoxygenation (H/R) in H9C2 and AC16 cells. Further, compared to wild-type mice, genetic deletion of Diaph1 reduced infarct size and improved contractile function after I/R. Silencing Diaph1 in H9C2 cells subjected to H/R downregulated actin polymerization and serum response factor-regulated gene expression. Importantly, these changes led to increased expression of sarcoplasmic reticulum Ca2+ ATPase and reduced expression of the sodium calcium exchanger. This work demonstrates that DIAPH1 is required for the myocardial response to I/R, and that targeting DIAPH1 may represent an adjunctive approach for myocardial salvage after acute infarction.

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