Open AccessTreatment with placental growth factor attenuates myocardial ischemia/reperfusion injury
Author(s) -
Yabing Zhang,
Yin Cao,
Jiang Xin,
Ping Lv,
Dongxu Chen,
Shiyue Li,
Hui Yang,
Chan Chen,
Bin Liu,
Qian Li
Publication year - 2018
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0202772
Subject(s) - oxidative stress , reperfusion injury , placental growth factor , apoptosis , reactive oxygen species , ischemia , medicine , mitochondrion , endocrinology , andrology , chemistry , biology , microbiology and biotechnology , vascular endothelial growth factor , biochemistry , vegf receptors
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.