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Effects of platelet-derived growth factor-AA and -BB on embryonic cardiac development
Robert L Price1, Stephen T Haley, Tara A Bullard
1Department of Developmental Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, South Carolina, USA.
Insights
Platelet-derived growth factor (PDGF) exposure enhances embryonic heart development. Increased PDGF-AA or -BB accelerates myocardial differentiation and protein synthesis, promoting healthier cardiac myocyte development.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Cell Signaling
Background:
- Platelet-derived growth factor (PDGF) signaling is crucial for embryonic development, with disruptions leading to cardiac defects.
- The precise role of PDGF in cardiac myocyte differentiation remains incompletely understood.
Purpose of the Study:
- To investigate the specific effects of PDGF-AA and PDGF-BB ligands on embryonic cardiac myocyte differentiation and heart development.
- To elucidate the impact of exogenous PDGF on myocardial growth and maturation.
Main Methods:
- Whole-embryo culture (WEC) of rat and mouse embryos with controlled exposure to PDGF-AA or PDGF-BB ligands.
- Analysis of heart growth parameters (e.g., ventricular length, width) and total protein levels.
- Microscopic examination (confocal and transmission electron microscopy) to assess myocyte differentiation and sarcomere organization.
Main Results:
- PDGF-AA exposure increased cardiac total protein by 42% and enhanced myofibrillar bundle size and number.
- PDGF-BB exposure increased cardiac total protein by 77% and significantly improved heart parameters by 8-15%.
- Both PDGF-AA and PDGF-BB promoted increased sarcomere presence and myofibril differentiation in the myocardium.
Conclusions:
- Increased embryonic exposure to PDGF-AA or PDGF-BB accelerates the rate of myocardial development.
- PDGF signaling plays a significant role in promoting cardiac myocyte differentiation and maturation during embryogenesis.
- Exogenous PDGF administration can enhance embryonic cardiac growth and differentiation.
Abstract:
Several studies have shown that disruption of the normal expression patterns of platelet-derived growth factor (PDGF) ligands and receptors during development results in gross cardiac defects and embryonic or neonatal death. However, little is known about the specific role that PDGF plays in the differentiation of cardiac myocytes. In experiments complementing studies that utilized naturally-occurring Patch mice lacking the PDGFr alpha, or knockout animals lacking a PDGF ligand or receptor, we used rat and mouse whole-embryo culture (WEC) techniques to increase the exposure of embryos to the PDGF-AA or -BB ligands. Following a 48-hr culture period, we analyzed heart growth and cardiac myocyte differentiation. Exposure of rat embryos to 50 ng/ml of PDGF-AA resulted in a 42% increase in total protein levels in the heart, but did not result in a significant increase in heart growth, as determined by measurements of the atrioventricular length and the left ventricular length and width. Exposure of embryos to 50 ng/ml of PDGF-BB resulted in a 77% increase in total protein levels and a significant (P < 0.05) 8-15% increase in the measured heart parameters. Although a comparison of control and PDGF-AA-treated embryos showed no increase in the overall size of the heart, confocal microscopy showed an increase in the size and number of myofibrillar bundles in the developing myocardium. In addition, transmission electron microscopy (TEM) revealed an increase in the presence of sarcomeres, indicating that myofibrils were more highly differentiated in these areas of the treated embryos. In PDGF-BB-treated embryos, the compact zone of the myocardium was thicker and, as shown by confocal microscopy and TEM, f-actin and well-developed sarcomeres were more prevalent, indicating that the myofibrils were more differentiated in the treated embryos than in the control embryos. These studies indicate that increased exposure of embryonic hearts to PDGF-AA or -BB increases the rate of myocardial development.