Abstract
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.
Highlights
Swiprosin-1, known as EF-Hand domain family member D2 (EFhd2), acts as a calcium sensor that stabilizes F-actin filaments by blocking binding sites of cofilin [1]
We first investigated the expression of swiprosin-1 in post-myocardial infarction (MI) hearts
Experiments were performed on mouse hearts previously used for investigating the role of oncostatin M in cardiac repair, because in cultured cardiomyocytes swiprosin-1 and oncostatin M are coregulated
Summary
Swiprosin-1, known as EF-Hand domain family member D2 (EFhd2), acts as a calcium sensor that stabilizes F-actin filaments by blocking binding sites of cofilin [1]. A drosophila-specific homologue of human swiprosin-1 participates in skeletal muscle formation [10]. In immune cells, it triggers the formation of lamellopodia, which is required for migration of macrophages [11]. Swiprosin-1 is required for the formation of pseudopodia-like structures [9,12]. Extensive cardiac remodeling with global cardiac changing in gene expression occurs subsequently to myocardial infarction (MI) when repair processes occur [13,14,15]. In the present study we investigated the expression of swiprosin-1 in cardiac tissue during subsequent cardiac remodeling
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