scholarly journals Snake Venom Vascular Endothelial Growth Factors (VEGFs) Exhibit Potent Activity through Their Specific Recognition of KDR (VEGF Receptor 2)

2003 ◽  
Vol 278 (52) ◽  
pp. 51985-51988 ◽  
Author(s):  
Yasuo Yamazaki ◽  
Koji Takani ◽  
Hideko Atoda ◽  
Takashi Morita
Keyword(s):  
Growth Factors ◽  
Snake Venom ◽  
Vascular Endothelial Growth Factors ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Specific Recognition ◽  
Endothelial Growth Factors

scholarly journals Hypotensive Snake Venom Components—A Mini-Review

Molecules ◽  
2019 ◽  
Vol 24 (15) ◽  
pp. 2778 ◽  
Author(s):  
Orsolya Péterfi ◽  
Francisc Boda ◽  
Zoltán Szabó ◽  
Elek Ferencz ◽  
László Bába
Keyword(s):  
Blood Pressure ◽  
Growth Factors ◽  
Snake Venom ◽  
Natriuretic Peptides ◽  
Kidney Diseases ◽  
Public Health Issue ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Phospholipases A2 ◽  
Endothelial Growth Factors

Hypertension is considered a major public health issue due to its high prevalence and subsequent risk of cardiovascular and kidney diseases. Thus, the search for new antihypertensive compounds remains of great interest. Snake venoms provide an abundant source of lead molecules that affect the cardiovascular system, which makes them prominent from a pharmaceutical perspective. Such snake venom components include bradykinin potentiating peptides (proline-rich oligopeptides), natriuretic peptides, phospholipases A2, serine-proteases and vascular endothelial growth factors. Some heparin binding hypotensive factors, three-finger toxins and 5′ nucleotidases can also exert blood pressure lowering activity. Great advances have been made during the last decade regarding the understanding of the mechanism of action of these hypotensive proteins. Bradykinin potentiating peptides exert their action primarily by inhibiting the angiotensin-converting enzyme and increasing the effect of endogenous bradykinin. Snake venom phospholipases A2 are capable of reducing blood pressure through the production of arachidonic acid, a precursor of cyclooxygenase metabolites (prostaglandins or prostacyclin). Other snake venom proteins mimic the effects of endogenous kallikrein, natriuretic peptides or vascular endothelial growth factors. The aim of this work was to review the current state of knowledge regarding snake venom components with potential antihypertensive activity and their mechanisms of action.

Snake venom vascular endothelial growth factors (svVEGFs): unravelling their molecular structure, functions, and research potential

2021 ◽  
Author(s):  
Isabela Gobbo Ferreira ◽  
Manuela Berto Pucca ◽  
Isadora Sousa de Oliveira ◽  
Felipe Augusto Cerni ◽  
Beatriz de Cássia da Silva Jacob ◽  
...  
Keyword(s):  
Molecular Structure ◽  
Growth Factors ◽  
Snake Venom ◽  
Structure Functions ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Endothelial Growth Factors

scholarly journals Snake Venom Vascular Endothelial Growth Factors (VEGF-Fs) Exclusively Vary Their Structures and Functions among Species

2009 ◽  
Vol 284 (15) ◽  
pp. 9885-9891 ◽  
Author(s):  
Yasuo Yamazaki ◽  
Yukiko Matsunaga ◽  
Yuko Tokunaga ◽  
Shinya Obayashi ◽  
Mai Saito ◽  
...  
Keyword(s):  
Growth Factors ◽  
Snake Venom ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Endothelial Growth Factors

scholarly journals The cellular response to vascular endothelial growth factors requires co-ordinated signal transduction, trafficking and proteolysis

2015 ◽  
Vol 35 (5) ◽  
Author(s):  
Gina A. Smith ◽  
Gareth W. Fearnley ◽  
Darren C. Tomlinson ◽  
Michael A. Harrison ◽  
Sreenivasan Ponnambalam
Keyword(s):  
Signal Transduction ◽  
Growth Factors ◽  
Membrane Trafficking ◽  
Cellular Response ◽  
Signal Transduction Pathways ◽  
Vascular Endothelial Growth Factors ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Wide Range ◽  
Endothelial Growth Factors

VEGFs (vascular endothelial growth factors) are a family of conserved disulfide-linked soluble secretory glycoproteins found in higher eukaryotes. VEGFs mediate a wide range of responses in different tissues including metabolic homoeostasis, cell proliferation, migration and tubulogenesis. Such responses are initiated by VEGF binding to soluble and membrane-bound VEGFRs (VEGF receptor tyrosine kinases) and co-receptors. VEGF and receptor splice isoform diversity further enhances complexity of membrane protein assembly and function in signal transduction pathways that control multiple cellular responses. Different signal transduction pathways are simultaneously activated by VEGFR–VEGF complexes with membrane trafficking along the endosome–lysosome network further modulating signal output from multiple enzymatic events associated with such pathways. Balancing VEGFR–VEGF signal transduction with trafficking and proteolysis is essential in controlling the intensity and duration of different intracellular signalling events. Dysfunction in VEGF-regulated signal transduction is important in chronic disease states including cancer, atherosclerosis and blindness. This family of growth factors and receptors is an important model system for understanding human disease pathology and developing new therapeutics for treating such ailments.

scholarly journals Proteolytic Cleavages in the VEGF Family: Generating Diversity among Angiogenic VEGFs, Essential for the Activation of Lymphangiogenic VEGFs

Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 167
Author(s):  
Jaana Künnapuu ◽  
Honey Bokharaie ◽  
Michael Jeltsch
Keyword(s):  
Growth Factors ◽  
Molecular Level ◽  
Specific Antigen ◽  
Receptor Activation ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Turn On ◽  
C And N ◽  
Proteolytic Cleavages ◽  
Endothelial Growth Factors

Specific proteolytic cleavages turn on, modify, or turn off the activity of vascular endothelial growth factors (VEGFs). Proteolysis is most prominent among the lymph­angiogenic VEGF-C and VEGF-D, which are synthesized as precursors that need to undergo enzymatic removal of their C- and N-terminal propeptides before they can activate their receptors. At least five different proteases mediate the activating cleavage of VEGF-C: plasmin, ADAMTS3, prostate-specific antigen, cathepsin D, and thrombin. All of these proteases except for ADAMTS3 can also activate VEGF-D. Processing by different proteases results in distinct forms of the “mature” growth factors, which differ in affinity and receptor activation potential. The “default” VEGF-C-activating enzyme ADAMTS3 does not activate VEGF-D, and therefore, VEGF-C and VEGF-D do function in different contexts. VEGF-C itself is also regulated in different contexts by distinct proteases. During embryonic development, ADAMTS3 activates VEGF-C. The other activating proteases are likely important for non-developmental lymphangiogenesis during, e.g., tissue regeneration, inflammation, immune response, and pathological tumor-associated lymphangiogenesis. The better we understand these events at the molecular level, the greater our chances of developing successful therapies targeting VEGF-C and VEGF-D for diseases involving the lymphatics such as lymphedema or cancer.

scholarly journals Study of Microvessel Density and the Expression of Vascular Endothelial Growth Factors in Adrenal Gland Pheochromocytomas

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Magdalena Białas ◽  
Grzegorz Dyduch ◽  
Joanna Dudała ◽  
Monika Bereza-Buziak ◽  
Alicja Hubalewska-Dydejczyk ◽  
...  
Keyword(s):  
Growth Factors ◽  
Microvessel Density ◽  
Antiangiogenic Therapy ◽  
Prognostic Significance ◽  
Operation Technique ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Vascular Architecture ◽  
Laparoscopic Operation ◽  
Endothelial Growth Factors

Angiogenesis (neoangiogenesis), a process of neovascularization, is an essential step for local tumor growth and distant metastasis formation. We have analysed angiogenesis status: vascular architecture, microvessel density, and vascular endothelial growth factors expression in 62 adrenal pheochromocytomas: 57 benign and 5 malignant. Immunohistochemical evaluation revealed that vascular architecture and vessel density are different in the central and subcapsular areas of the tumor. Furthermore, we have observed a strong correlation between number of macrophages and microvessel density in the central and subcapsular areas of the tumor and between the expression of VEGF-A in tumor cells and microvessel density in central and subcapsular areas of the tumor. Secondary changes in these tumors influence the results and both vascular architecture and microvessel density are markedly disturbed by hemorrhagic and cystic changes in pheochromocytomas. These changes are partially caused by laparoscopic operation technique. However, no differences in vascular parameters were found between pheochromocytomas with benign and malignant clinical behavior. Our observation showed that analysis of angiogenesis, as a single feature, does not help in differentiating malignant and benign pheochromocytomas and has no independent prognostic significance. On the other hand, high microvessel density in pheochromocytoma is a promising factor for antiangiogenic therapy in malignant cases.

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