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Controlled Delivery of Angiogenic Proteins
Published in Emmanuel Opara, Controlled Drug Delivery Systems, 2020
Binita Shrestha, Jacob Brown, Eric M. Brey
Vascular Endothelial Growth Factors (VEGFs) are a family of factors that are required for angiogenesis and/or lymphangiogenesis (formation of lymphatic vessels). The VEGF family consists of a number of members, including VEGF-A (which has many isoforms), VEGF-B, VEGF-C, VEGF-D, and placental growth factor (PIGF) [20]. Each of these members play important, but often different, roles in biological processes. For example, VEGF-A binds with VEGFR-1 to regulate normal and pathological angiogenesis. VEGF-A also binds with VEGFR-2 to modulate growth, migration, survival, and permeability of ECs [21] and stimulates ECs to release other growth factors essential to activate surrounding cells [22]. VEGF-C and VEGF-D and their receptor VEGFR-3 have been reported to regulate lymphangiogenesis. There is also a subgroup of VEGF isolated from snake venom, VEGF-F. VEGF-F regulates vascular permeability, angiogenesis, and blood pressure [23]. PIGF binds specifically to VEGFR-1 and regulates vascular events in both angiogenesis and vasculogenesis [24].
Overview of Angiogenesis: Molecular and Structural Features
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Arye Elfenbein, Michael Simons
VEGFR-1 (also named Flt-1) preferentially binds VEGF-A, VEGF-B and PlGF. VEGFR-2 (also named KDR/Flk-1) is a receptor for VEGF-A, -C and –D; it is predominantly involved in orchestrating the VEGF-specific effects of vascular growth and increased permeability (8). Variants of these receptors that consist only of the soluble extracellular domain exist physiologically (9). These soluble receptors serve as membrane receptor antagonists by sequestering nearby VEGF molecules and are therefore functionally angiostatic. Finally, the last member of the high-affinity VEGF receptors is VEGF-3, which binds VEGF-C and -D. This receptor has been reported to contribute to embryonic vessel maturation, yet its role in the adult is mostly limited to, and critical for, lymphatic system growth (10).
Imaging Angiogenesis
Published in George C. Kagadis, Nancy L. Ford, Dimitrios N. Karnabatidis, George K. Loudos, Handbook of Small Animal Imaging, 2018
VEGF actions in angiogenesis are mediated through the VEGF receptors (VEGFR1 and VEGFR2) expressed on endothelial cells. To study these interactions, several transgenic animal models have been recently developed. A prime example of such a model is a VEGFR2-luciferase transgenic mouse model, in which luciferase expression is controlled by the VEGFR2 promoter region causing endothelial cells within angiogenic vasculature to express luciferase. This model has been validated in numerous studies including a cutaneous wound-healing model, in which the increase in luciferase signal (and thus VEGFR2 gene activation) peaked at 7–10 days after the wound was inflicted (Zhang et al. 2004).
Two trisimidazole-based coordination polymers: application values on breast cancer combined with psychological counseling
Published in Inorganic and Nano-Metal Chemistry, 2021
Qian Shi, Jing Wang, Hai-Li Zhang
The role of vascular endothelial growth factor (VEGF) signaling in cancer is not only well known in the context of angiogenesis, but also important in the regulation of tumor cell functions.[1] VEGF was originally discovered to promote endothelial growth and increase the production of proteins that increase blood vessel permeability.[2] For these reasons, the role of VEGF in cancer is expected to be limited to angiogenesis. However, it is now obvious that VEGF has functions unrelated to angiogenesis in specific receptor-mediated cancers.[3] Tumor cells express VEGF receptor tyrosine kinases (VEGFR1 and VEGFR2) and neurofibrillin (NRP).