In utero angiopoietin-2 gene delivery remodels placental blood vessel phenotype: a murine model for studying placental angiogenesis

التفاصيل البيبلوغرافية
العنوان: In utero angiopoietin-2 gene delivery remodels placental blood vessel phenotype: a murine model for studying placental angiogenesis
المؤلفون: Eli Geva, P.C. Ursell, D.H. Moore, R.B. Jaffe, D.G. Ginzinger
المصدر: MHR: Basic science of reproductive medicine. 11:253-260
بيانات النشر: Oxford University Press (OUP), 2005.
سنة النشر: 2005
مصطلحات موضوعية: Transcriptional Activation, Embryology, Transcription, Genetic, Angiogenesis, Placenta, Genetic Vectors, Neovascularization, Physiologic, Biology, Transfection, Vascular remodelling in the embryo, Angiopoietin-2, Extracellular matrix, Angiopoietin, Mice, chemistry.chemical_compound, Pregnancy, Genetics, medicine, Animals, Humans, RNA, Messenger, Molecular Biology, Obstetrics and Gynecology, Cell Biology, Placentation, Extracellular Matrix, Cell biology, Vascular endothelial growth factor, Endothelial stem cell, Phenotype, medicine.anatomical_structure, Reproductive Medicine, chemistry, Models, Animal, Immunology, cardiovascular system, Blood Vessels, Female, Endothelium, Vascular, Developmental Biology, Blood vessel
الوصف: Angiopoietin (Ang)-2, the natural antagonist of the Ang1/Tie2 receptor is a complex regulator of blood vessel plasticity that plays a pivotal role in both vessel sprouting [in the presence of vascular endothelial growth factor (VEGF)-A] and vessel regression (in the absence of VEGF-A). Based on the spatial and temporal expression of Ang2 throughout human gestation, we recently suggested that the Ang2 may play a pivotal role in placental angiogenesis. Further, to examine this tenet we have developed a novel murine model system in which in utero Ang2 gene delivery via a non-replicating adenoviral expression vector has the potential to manipulate the blood vessel phenotype in vivo during pregnancy. Ang2 overexpression selectively and rapidly remodels the labyrinth perivascular extracellular matrix, subsequently promoting plasticity of the maternal and fetal vessels, which appear honeycombed due to a 2-fold increase in blood vessel luminal area. High levels of Ang2 impair endothelial cell adhesiveness, leading to vascular leakiness with perivascular oedema, which increases placental weight. These observations suggest that the Ang2 overexpression may play a key role in placental vascular remodelling. Furthermore, we suggest a novel new model to study the pathobiology of placental vascularization and the effect of placental blood vessels on fetal phenotype.
تدمد: 1460-2407
1360-9947
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c8488bfa4c5fc7d3dd989e933ff2b4a1
https://doi.org/10.1093/molehr/gah159
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....c8488bfa4c5fc7d3dd989e933ff2b4a1
قاعدة البيانات: OpenAIRE