Premium
Stromal Interaction Molecule 1 Disruption Protects Myocardial from Ischemia ‐ Reperfusion Injury
Author(s) -
Mali Vishal R,
Ali Maha,
Haddox Samuel,
Belmadani Souad,
Trebak Mohamed,
Matrougui Khalid
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.952.5
Subject(s) - stim1 , endoplasmic reticulum , reperfusion injury , ischemia , downregulation and upregulation , medicine , stromal cell , myocardial infarction , chemistry , microbiology and biotechnology , cardiology , biology , biochemistry , gene
Background It has been reported that the increase in Stromal Interacting Molecule 1 (STIM1) expression is associated with myocardial complication. However, the role of vascular STIM1 in cardiac ischemia‐reperfusion (I/R) injury is unknown. Therefore, the central hypothesis of the present study is to determine the role of deleted STIM1 in endothelial cells or smooth muscle cells (SMC) in cardiac I/R injury. Thus, we performed cardiac I/R in control mice, mice lacking the STIM1 specifically in endothelial cells (Stim1 −/−EC ) or specifically in SMC (Stim1 −/−SMC ). Methods and Results All mice were subjected to cardiac ischemia for 40 minutes and followed by reperfusion for 24 hours. After 24 hours reperfusion, hearts were incubated with triphenyl tetrazolium chloride to determine the infarct size. In control mice subjected to I/R, the heart develops infarct, which represents 50% of the heart area. Interestingly, in Stim1 −/−EC and Stim1 −/−SMC , the infarct size was significantly reduced indicating that STIM1 disruption specifically in endothelial cells or SMC protects the heart from I/R injury. Importantly, the heart protection was greater in Stim1 −/−SMC than Stim1 −/−EC mice. We found an increase in the endoplasmic reticulum (ER) stress in control mice subjected to I/R than in Stim1 −/−SMC and Stim1 −/−EC mice subjected to I/R. Conclusion Our results indicate that STIM1 disruption in endothelial cells and SMC protects the heart from I/R injury likely through the inhibition of ER stress. Support or Funding Information NIH