Abstract
Studies have established that oxidative stress plays an important role in the pathology of myocardial ischemia/reperfusion injury (MIRI). Vascular endothelial growth factor receptor 1 (VEGFR1) activation was reported to reduce oxidative stress and apoptosis. In the present study, we tested the hypothesis that the activation of VEGFR1 by placental growth factor (PlGF) could reduce MIRI by regulating oxidative stress. Mouse hearts and neonatal mouse cardiomyocytes were subjected to ischemia/reperfusion (I/R) and oxygen glucose deprivation (OGD), respectively. PlGF pretreatment markedly ameliorated I/R injury, as demonstrated by reduced infarct size and improved cardiac function. The protection was associated with a reduction of cardiomyocyte apoptosis. Similarly, our in vitro study showed that PlGF treatment improved cell viability and reduced cardiomyocyte apoptosis. Also, activation of VEGFR1 by PlGF suppressed intracellular and mitochondrial reactive oxygen species (ROS) generation. However, VEGFR1 neutralizing monoclonal antibody, which preventing PlGF binding, totally blocked this protective effect. In conclusion, activation of VEGFR1 could protect heart from I/R injury by suppression of oxidative stress and apoptosis.
Highlights
Coronary heart disease is the leading cause of morbidity and mortality in the world.[1]
We investigated the effect of exogenous placental growth factor (PlGF) protein on cardiac function and prognosis after myocardial ischemia/reperfusion (I/R) and determined the role of PlGF-Vascular endothelial growth factor receptor 1 (VEGFR1) in oxidative stress of cardiomyocyte induced by hypoxia/reoxygenation (H/R)
We demonstrated that the activation of VEGFR1 by PlGF played a pivotal role in ameliorating myocardial ischemia/reperfusion injury” (MIRI)
Summary
Coronary heart disease is the leading cause of morbidity and mortality in the world.[1] After an acute myocardial infarction (AMI), the most effective strategy for reducing the size of a myocardial infarct and improving the clinical outcome is early and successful myocardial reperfusion. Placental growth factor and myocardial ischemia/reperfusion injury irreversible cell death by apoptosis and necrosis.[5,6,7] Presence of ROS in excess of the antioxidant capacity of the heart is one of the main mechanisms underlying the pathology of MIRI.[4, 8] As such, the oxidative stress is considered to be of paramount importance for MIRI development
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