scholarly journals Physiological Role of Vascular Endothelial Growth Factors as Homeostatic Regulators

2018 ◽  
pp. 955-979 ◽  
Author(s):  
David O. Bates ◽  
Nicholas Beazley-Long ◽  
Andrew V. Benest ◽  
Xi Ye ◽  
Nikita Ved ◽  
...  
Keyword(s):  
Growth Factors ◽  
Physiological Role ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Endothelial Growth Factors

scholarly journals Role of hypoxia and vascular endothelial growth factors in lymphangiogenesis

2014 ◽  
Vol 1 (1) ◽  
pp. e29907 ◽  
Author(s):  
Florent Morfoisse ◽  
Edith Renaud ◽  
Fransky Hantelys ◽  
Anne-Catherine Prats ◽  
Barbara Garmy-Susini
Keyword(s):  
Growth Factors ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Endothelial Growth Factors

scholarly journals Role of hypoxia and vascular endothelial growth factors in lymphangiogenesis

2015 ◽  
Vol 2 (4) ◽  
pp. e1024821 ◽  
Author(s):  
Florent Morfoisse ◽  
Edith Renaud ◽  
Fransky Hantelys ◽  
Anne-Catherine Prats ◽  
Barbara Garmy-Susini
Keyword(s):  
Growth Factors ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Endothelial Growth Factors

scholarly journals KLK3 in the Regulation of Angiogenesis—Tumorigenic or Not?

2021 ◽  
Vol 22 (24) ◽  
pp. 13545
Author(s):  
Hannu Koistinen ◽  
Jaana Künnapuu ◽  
Michael Jeltsch
Keyword(s):  
Growth Factors ◽  
Prostate Specific Antigen ◽  
Proteolytic Activity ◽  
Specific Antigen ◽  
Vascular Endothelial Growth Factors ◽  
Vascular Endothelial ◽  
Endothelial Growth Factors

In this focused review, we address the role of the kallikrein-related peptidase 3 (KLK3), also known as prostate-specific antigen (PSA), in the regulation of angiogenesis. Early studies suggest that KLK3 is able to inhibit angiogenic processes, which is most likely dependent on its proteolytic activity. However, more recent evidence suggests that KLK3 may also have an opposite role, mediated by the ability of KLK3 to activate the (lymph)angiogenic vascular endothelial growth factors VEGF-C and VEGF-D, further discussed in the review.

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.

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