scholarly journals Novel human Ab against vascular endothelial growth factor receptor 2 shows therapeutic potential for leukemia and prostate cancer

2019 ◽  
Vol 110 (12) ◽  
pp. 3773-3787 ◽  
Author(s):  
Ruei‐Min Lu ◽  
Chiung‐Yi Chiu ◽  
I‐Ju Liu ◽  
Yu‐Ling Chang ◽  
Yaw‐Jen Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Therapeutic Potential ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Relaxin Induces Rapid Dilation of Rodent Small Renal and Human Subcutaneous Arteries via PI3 Kinase and Nitric Oxide

Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2786-2796 ◽  
Author(s):  
Jonathan T. McGuane ◽  
Julianna E. Debrah ◽  
Laura Sautina ◽  
Yagna P. R. Jarajapu ◽  
Jacqueline Novak ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Therapeutic Potential ◽  
Growth Factor Receptor ◽  
Peptide Hormone ◽  
Mesenteric Arteries ◽  
No Production ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

The peptide hormone relaxin is a potent vasodilator with therapeutic potential in diseases complicated by vasoconstriction, including heart failure. However, the molecular mediators and magnitude of vasodilation may vary according to duration of exposure and artery type. The objective of these studies was to determine mechanisms of rapid (within minutes) relaxin-induced vasodilation and to examine whether relaxin dilates arteries from different animal species and vascular beds. Rat and mouse small renal, rat mesenteric, and human sc arteries were isolated, mounted in a pressure arteriograph, and treated with recombinant human relaxin (rhRLX; 1–100 ng/ml) after preconstriction with phenylephrine. Rat and mouse small renal as well as human sc arteries dilated in response to rhRLX, whereas rat mesenteric arteries did not. Endothelial removal or pretreatment with l-NG-monomethyl arginine (L-NMMA) abolished rapid relaxin-induced vasodilation; phosphatidylinositol-3-kinase (PI3K) inhibitors also prevented it. In cultured human endothelial cells, rhRLX stimulated nitric oxide (assessed using 4-amino-5-methylamino-2′7′-difluorofluorescein) as well as Akt and endothelial NO synthase (eNOS) phosphorylation by Western blotting but not increases in intracellular calcium (evaluated by fura-2). NO production was attenuated by inhibition of Gαi/o and Akt (using pertussis toxin and the allosteric inhibitor MK-2206, respectively), PI3K, and NOS. Finally, the dilatory effect of rhRLX in rat small renal arteries was unexpectedly potentiated, rather than inhibited, by pretreatment with the vascular endothelial growth factor receptor inhibitor SU5416. We conclude that relaxin rapidly dilates select arteries across a range of species. The mechanism appears to involve endothelial Gαi/o protein coupling to PI3K, Akt, and eNOS but not vascular endothelial growth factor receptor transactivation or increased calcium.

scholarly journals Gene Therapy of Prostate Cancer with the Soluble Vascular Endothelial Growth Factor Receptor Fk1

2002 ◽  
Vol 1 (5) ◽  
pp. 548-553 ◽  
Author(s):  
Christian M. Becker ◽  
Filip A. Franebo ◽  
Irina Iordanescu ◽  
Danielle J. Behonick ◽  
Mei-Chiung Shih ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Gene Therapy ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Aberrant methylation of the vascular endothelial growth factor receptor-1 gene in prostate cancer

2003 ◽  
Vol 94 (6) ◽  
pp. 536-539 ◽  
Author(s):  
Yasushi Yamada ◽  
Masatoshi Watanabe ◽  
Mikio Yamanaka ◽  
Yoshifumi Hirokawa ◽  
Hiroyoshi Suzuki ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Aberrant Methylation ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor
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