Swiprosin-1/EFhD-2 Expression in Cardiac Remodeling and Post-Infarct Repair: Effect of Ischemic Conditioning.
Zoltán GiriczAndrás MakkosRolf SchreckenbergJochen PölingHolger LörchnerKrisztina KissPéter BencsikThomas BraunRainer SchulzPéter FerdinandyKlaus-Dieter SchlüterPublished in: International journal of molecular sciences (2020)
Swiprosin-1 (EFhD2) is a molecule that triggers structural adaptation of isolated adult rat cardiomyocytes to cell culture conditions by initiating a process known as cell spreading. This process mimics central aspects of cardiac remodeling, as it occurs subsequent to myocardial infarction. However, expression of swiprosin-1 in cardiac tissue and its regulation in vivo has not yet been addressed. The expression of swiprosin-1 was analyzed in mice, rat, and pig hearts undergoing myocardial infarction or ischemia/reperfusion with or without cardiac protection by ischemic pre- and postconditioning. In mouse hearts, swiprosin-1 protein expression was increased after 4 and 7 days in myocardial infarct areas specifically in cardiomyocytes as verified by immunoblotting and histology. In rat hearts, swiprosin-1 mRNA expression was induced within 7 days after ischemia/reperfusion but this induction was abrogated by conditioning. As in cultured cardiomyocytes, the expression of swiprosin-1 was associated with a coinduction of arrestin-2, suggesting a common mechanism of regulation. Rno-miR-32-3p and rno-miR-34c-3p were associated with the regulation pattern of both molecules. Moreover, induction of swiprosin-1 and ssc-miR-34c was also confirmed in the infarct zone of pigs. In summary, our data show that up-regulation of swiprosin-1 appears in the postischemic heart during cardiac remodeling and repair in different species.
Keyphrases
- left ventricular
- poor prognosis
- long non coding rna
- acute myocardial infarction
- heart failure
- cell proliferation
- high glucose
- oxidative stress
- ischemia reperfusion injury
- binding protein
- endothelial cells
- long noncoding rna
- cerebral ischemia
- single cell
- machine learning
- young adults
- percutaneous coronary intervention
- atrial fibrillation
- metabolic syndrome
- insulin resistance
- diabetic rats