Abstract
The BPH/5 mouse model spontaneously develops the hallmarks of PE, including fetoplacental abnormalities and an imbalance in pro‐and anti‐angiogenic factors. We have utilized ultrasonography to categorize BPH/5 fetoplacental units (FPUs) at e10.5 into three increasingly severe phenotypic classes (I, II and III). We previously demonstrated that thrombospondin 2 (Thbs2), an inhibitor of angiogenesis, is significantly increased in BPH/5 Class II and III FPUs compared to C57. To further understand the mechanism of Thbs2 in BPH/5 FPUs, we hypothesized that Thbs2 could either activate apoptosis signaling pathways via CD36 or block angiogenesis signaling through interaction of CD47 and VEGFR2. Real time qPCR results show that CD36 mRNA expression was significantly increased in BPH/5 Class II and III FPUs (II=2.8 ± 0.42; III=3.2 ± 0.1 fold vs C57, n=3, p<0.05), while CD47 (1.5 ± 0.15 fold vs C57, n=3, p<0.05) and VEGFR2 (1.7 ± 0.17 fold vs C57, n=3, p<0.05) were up‐regulated in BPH/5 Class II FPUs. Western analysis confirmed that CD47 protein expression was increased in BPH/5 FPUs. We conclude that Thbs2 may exert its effects on fetoplacental development in BPH/5 via CD36 and CD47 receptors. Funding: QNRF NPRP09‐1099‐279.
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