A role for Sfrp2 in cardiomyogenesis in vivo
Year: 2021
Type: article
Abstract: Cardiomyogenesis, the process by which the body generates cardiomyocytes, is poorly understood. We have recently shown that Sfrp2 promotes cardiomyogenesis in vitro. The objective of this study was to determine if Sfrp2 would similarly promote cardiomyogenesis in vivo. To test this hypothesis, we tracked multipotent cKit(+) cells in response to Sfrp2 treatment. In control adult mice, multipotent cKit(+) cells typically differentiated into endothelial cells but not cardiomyocytes. In contrast, Sfrp2 switched the fate of these cells. Following Sfrp2 injection, multipotent cKit(+) cells differentiated solely into cardiomyocytes. Sfrp2-derived cardiomyocytes integrated into the myocardium and exhibited identical physiological properties to preexisting native cardiomyocytes. The ability of Sfrp2 to promote cardiomyogenesis was further supported by tracking EdU-labeled cells. In addition, Sfrp2 did not promote the formation of new cardiomyocytes when the cKit(+) cell population was selectively ablated in vivo using a diphtheria toxin receptor-diphtheria toxin model. Notably, Sfrp2-induced cardiomyogenesis was associated with significant functional improvements in a cardiac injury model. In summary, our study further demonstrates the importance of Sfrp2 in cardiomyogenesis.
Authors: José A. Gomez, Alan Payne, Richard E. Pratt, Conrad P. Hodgkinson, Victor J. Dzau
Institutions: Duke Medical Center, Vanderbilt University Medical Center
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Awards: Gene Therapy for Long-Term Myocardial Protection, Renin Gene Expression in Cardiovascular Regulation: Mechanisms of JG Hyperplasia, G6483445886, Genetically Altered Mesenchymal Stem Cell; Paracrine Effect on Neovascularization, Sfrp2 and Cardiac Progenitor Cells in Regenerative Response to Ischemic Injury
OpenAlex ID: W3192290017