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Published on: October 19, 2013
Hypoxia increases placenta growth factor expression in human myocardium and cultured neonatal rat cardiomyocytes
Ronald J Torry1, Robert J Tomanek, Wei Zheng
1College of Pharmacy and Health Sciences, Drake University, Des Moines, Iowa 50311-4505, USA. ron.torry@drake.edu
Insights
Placenta growth factor (PlGF) in cardiomyocytes increases with hypoxia and myocardial damage, suggesting a role in cardiac healing after ischemia.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Regenerative Medicine
Background:
- Placenta growth factor (PlGF) is implicated in pathological angiogenesis and serves as a biomarker in coronary artery disease.
- Limited understanding exists regarding PlGF expression regulation within cardiac tissue.
Purpose of the Study:
- To investigate the regulation of PlGF and its receptor, VEGFR1, in human cardiac allografts.
- To examine PlGF and VEGFR1 expression in cardiomyocytes under hypoxic and mechanical stress conditions.
Main Methods:
- Analysis of PlGF and VEGFR1 mRNA expression in human cardiac allograft biopsies.
- Assessment of PlGF and VEGFR1 in cultured neonatal rat cardiomyocytes subjected to hypoxia and cyclical stretch.
- Immunohistochemical localization of PlGF protein in cardiac tissue.
Main Results:
- PlGF and VEGFR1 mRNA were detected in normal and abnormal cardiac allografts.
- Biopsies with myocardial fibrin, elevated troponin I, and infiltrates showed increased PlGF mRNA.
- Hypoxia significantly upregulated PlGF expression in cultured cardiomyocytes, while cyclical stretch had no significant effect.
Conclusions:
- Cardiomyocyte PlGF expression is upregulated by hypoxia in vitro.
- Increased PlGF expression is observed in cardiac allografts with myocardial damage.
- Endogenous PlGF may play a role in cardiac repair following hypoxia or ischemia.
Background:
Placenta growth factor (PlGF) plays an important role in pathologic angiogenesis and is believed to be an independent biomarker in patients with coronary artery disease. However, little is known regarding the regulation of PlGF expression in heart tissue.
Methods:
We determined expression changes in PlGF and its receptor, VEGFR1, in normal and abnormal biopsies from human cardiac allografts and in cardiomyocytes cultured under hypoxia or cyclical stretch conditions.
Results:
Human donor myocardium and biopsies from allografts without fibrin deposits expressed PlGF and VEGFR1 mRNA. Biopsies (n = 7) with myocardial fibrin, elevated serum cardiac troponin I titers (p < 0.03) and cellular infiltrates (p < 0.05) expressed 1.6-fold more PlGF mRNA than biopsies from allografts without fibrin (n = 11; p < 0.05). PlGF protein was localized in cardiomyocytes, extracellular matrix and some microvessels in areas with fibrin deposition. VEGFR1 mRNA expression was not different between groups. Cultured neonatal rat cardiomyocytes constitutively expressed PlGF/VEGFR1 under normoxia. PlGF expression was increased 3.88 +/- 0.62-fold after 12 hours (n = 6; p
Conclusions:
Cardiomyocyte PIGF expression is upregulated by hypoxia in vitro and its expression increases significantly in allografts with myocardial damage. Collectively, these results provide important temporal and spatial evidence that endogenous PlGF may facilitate cardiac healing after myocardial hypoxia/ischemia.
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