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Placenta Growth Factor Expression and Function in Cultured Neonatal Rat Cardiomyocytes
Author(s) -
Torry Ronald,
Bohman Kyle,
Berendt Robert,
Sandquist Joshua,
Ronnebaum Sarah,
Torry Donald
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1189
Subject(s) - placental growth factor , apoptosis , medicine , angiogenesis , receptor , endocrinology , placenta , andrology , hypoxia (environmental) , fetus , vascular endothelial growth factor , chemistry , biology , pregnancy , vegf receptors , biochemistry , genetics , organic chemistry , oxygen
Placenta growth factor (PlGF) induces angiogenesis and protects placental trophoblast from apoptosis. However, little is known regarding the expression and function of PlGF in heart tissue. The present study sought to determine if: 1) cardiomyocytes (CMs) express the receptor for PlGF, 2) exogenous PlGF activates receptors on CMs, and 3) exogenous PlGF can protect CMs from hypoxia‐reoxygenation (H/R) or serum deprivation‐induced (SD) apoptosis. CMs were isolated from 2–4 day‐old rat pups, cultured and studied within 5 days of plating. RT‐PCR showed that CMs express PlGF and its receptor, VEGFR1, mRNA under normal culture conditions. Exogenous PlGF (10 ng/ml) produced a 4‐fold increase in ERK1/2 phosphorylation similar to that produced by VEGF165 (10 ng/ml). H/R was produced by placing plates in 1–2%O2 for 36 hours followed by normoxia for 6 hours. SD was induced by culturing the cells in media lacking FCS for 48 hours. PlGF (25 ng/ml) was added 8–12 hours prior to apoptotic insult and caspase‐3,7 enzymatic activity was assessed. SD produced a 1.56+0.18 fold increase (p<0.05) in caspase activity over control; this was reduced to 1.11+0.06 by pre‐treatment with PlGF (n=8; p<0.05 from SD). H/R produced a 1.62+0.42‐fold increase in caspase activity (n=6). PlGF pre‐treatment tended to decrease caspase activity (1.18+0.29 of control; n=2). Our results show that CMs express PlGF and its receptor, that the receptors are functional, and that pretreatment with PlGF protects CMs from some types of caspase‐dependent apoptosis. Supported by R15‐HL72802‐01 (RJT) and March of Dimes (DST).