Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene.
Napoleone Ferrara,Karen Carver-Moore,Helen Hsifei Chen,Mary Dowd,Lucy Lu,K. Sue O'Shea,Lyn Powell-Braxton,Kenneth J. Hillan,Mark W. Moore +8 more
TL;DR: The unexpected finding that loss of a single VEGF allele is lethal in the mouse embryo between days 11 and 12 was reported, and angiogenesis and blood-island formation were impaired, resulting in several developmental anomalies.
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Abstract: ANGIOGENESIS is required for a wide variety of physiological and pathological processes1. The endothelial cell-specific mitogen vascular endothelial growth factor (VEGF)2,3 is a major mediator of pathological angiogenesis4–6. Also, the expression of VEGF and its two receptors, Flt-1 and Flk-1/KDR, is related to the formation of blood vessels in mouse and rat embryos7–10. Mice homozygous for mutations that inactivate either receptor die in utero between days 8.5 and 9.5 (refs 11,12). However, ligand(s) other than VEGF might activate such receptors13,14. To assess the role of VEGF directly, we disrupted the VEGF gene in embryonic stem cells. Here we report the unexpected finding that loss of a single VEGF allele is lethal in the mouse embryo between days 11 and 12. Angiogenesis and blood-island formation were impaired, resulting in several developmental anomalies. Furthermore, VEGF-null embryonic stem cells exhibit a dramatically reduced ability to form tumours in nude mice.
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Interactions between VEGFR and Notch signaling pathways in endothelial and neural cells
Jean-Leon Thomas,Kasey L. Baker,Jinah Han,Charles Calvo,Harri Nurmi,Anne Eichmann,Kari Alitalo +6 more
TL;DR: This review will focus on Notch signaling in the vertebrate vascular and nervous systems and examine its role in angiogenesis, neurogenesis, and neurovascular interactions, and highlight the molecular relationships of the Notch pathway with vascular endothelial growth factors and their high-affinity tyrosine kinase VEGF receptors.
83
Bioactive electrospun fibers of poly(glycerol sebacate) and poly(ε-caprolactone) for cardiac patch application.
Ranjana Rai,Marwa Tallawi,Caterina Frati,Angela Falco,Andrea Gervasi,Federico Quaini,Judith A. Roether,Tobias Hochburger,Dirk W. Schubert,Lothar Seik,Niccoletta Barbani,Luigi Lazzeri,Elisabetta Rosellini,Aldo R. Boccaccini +13 more
TL;DR: The prospects of VEGF‐functionalized PGS–PCL fibrous scaffold as promising matrix for cardiac patch application are demonstrated and shown to be bioactive and biocompatible.
83
NF-kappaB contributes to transcription of placenta growth factor and interacts with metal responsive transcription factor-1 in hypoxic human cells.
Mirjam Cramer,Ivana Nagy,Brian J. Murphy,Max Gassmann,Michael O. Hottiger,Oleg Georgiev,Walter Schaffner +6 more
TL;DR: It is found that hypoxic conditions induce nuclear translocation and interaction of MTF-1 and NF-κB p65 proteins, suggesting a role for this complex in hypoxia-induced transcription of PlGF.
Considerations in assessing the developmental and reproductive toxicity potential of biopharmaceuticals
TL;DR: A case-by-case approach is needed for DART and general toxicity evaluation, which requires consideration of specific product attributes including biochemical and biophysical characteristics, pharmacological activity, and intended clinical indication.
83
Vascular Aging: Implications for Cardiovascular Disease and Therapy.
Yohannes T. Ghebre,Eduard Yakubov,Wing Tak Wong,Prasanna Krishnamurthy,Nazish Sayed,Andrew G. Sikora,Mark D. Bonnen +6 more
TL;DR: The impact of advancing age on cardiovascular health is discussed, and the cellular and molecular mechanisms that underlie age-associated vascular changes are highlighted.
82
References
Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice.
Fouad Shalaby,Janet Rossant,Janet Rossant,Terry P. Yamaguchi,Terry P. Yamaguchi,Marina Gertsenstein,Xiang-Fu Wu,Xiang-Fu Wu,Martin L. Breitman,Martin L. Breitman,Andre C. Schuh +10 more
TL;DR: The generation of mice deficient in Flk-1 by disruption of the gene using homologous recombination in embryonic stem (ES) cells is reported, indicating that FlK-1 is essential for yolk-sac blood-island formation and vasculogenesis in the mouse embryo.
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Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo
TL;DR: It is demonstrated that inhibition of the action of an angiogenic factor spontaneously produced by tumour cells may suppress tumour growth in vivo.
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Vascular Endothelial Growth Factor in Ocular Fluid of Patients with Diabetic Retinopathy and Other Retinal Disorders
Lloyd Paul Aiello,Robert L. Avery,Paul G. Arrigg,B A Keyt,Henry D. Jampel,Sweta Shah,Louis R. Pasquale,Hagen Thieme,Mami Iwamoto,John Edward Park +9 more
TL;DR: The data suggest that VEGF plays a major part in mediating active intraocular neovascularization in patients with ischemic retinal diseases, such as diabetic retinopathy and retinal-vein occlusion.
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•Journal Article
Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis.
TL;DR: T tumors have "borrowed" fundamental mechanisms that developed in multicellular organisms for purposes of tissue defense, renewal, and repair and taught us something new about angiogenesis, namely, that vascular hyperpermeability and consequent plasma protein extravasation are important, perhaps essential, elements in its generation.
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