Swiprosin-1/EFhD-2 Expression in Cardiac Remodeling and Post-Infarct Repair
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,...
Elmentve itt :
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| Dokumentumtípus: | Cikk |
| Megjelent: |
2020
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| Sorozat: | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
21 No. 9 |
| doi: | 10.3390/ijms21093359 |
| mtmt: | 31313455 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/18949 |
| Tartalmi kivonat: | 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. |
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| Terjedelem/Fizikai jellemzők: | Azonosító: 3359-Terjedelem: 13 p |
| ISSN: | 1661-6596 |