PTEN overexpression attenuates angiogenic processes of endothelial cells by blockade of endothelin-1/endothelin B receptor signaling

2012 ◽  
Vol 221 (2) ◽  
pp. 341-349 ◽  
Author(s):  
Hsiao-Mei Kuo ◽  
Chun-Yao Lin ◽  
Hing-Chung Lam ◽  
Pey-Ru Lin ◽  
Hoi-Hung Chan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Receptor Signaling ◽  
Endothelin B Receptor ◽  
Endothelin 1 ◽  
Endothelin B

scholarly journals Placenta growth factor augments endothelin-1 and endothelin-B receptor expression via hypoxia-inducible factor-1α

Blood ◽  
2008 ◽  
Vol 112 (3) ◽  
pp. 856-865 ◽  
Author(s):  
Nitin Patel ◽  
Caryn S. Gonsalves ◽  
Punam Malik ◽  
Vijay K. Kalra
Keyword(s):  
Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Receptor Expression ◽  
Placenta Growth Factor ◽  
Promoter Regions ◽  
Endothelin B Receptor ◽  
Endothelin 1 ◽  
Hypoxia Inducible Factor 1Α ◽  
Endothelin B ◽  
Potent Vasoconstrictor

Abstract Pulmonary hypertension (PHT) develops in sickle cell disease (SCD) and is associated with high mortality. We previously showed that erythroid cells produce placenta growth factor (PlGF), which activates monocytes to induce proinflammatory cytochemokines, contributing to the baseline inflammation and severity in SCD. In this study, we observed that PlGF increased expression of endothelin-1 (ET-1) and endothelin-B receptor (ET-BR) from human pulmonary microvascular endothelial cells (HPMVECs) and monocytes, respectively. PlGF-mediated ET-1 and ET-BR expression occurred via activation of PI-3 kinase, reactive oxygen species and hypoxia inducible factor-1α (HIF-1α). PlGF increased binding of HIF-1α to the ET-1 and ET-BR promoters; this effect was abrogated with mutation of hypoxia response elements in the promoter regions and HIF-1α siRNA and confirmed by chromatin immunoprecipitation analysis. Furthermore, PlGF-mediated ET-1 release from HPMVECs and ET-BR expression in monocytes creates a PlGF–ET-1–ET-BR loop, leading to increased expression of MCP-1 and IL-8. Our studies show that PlGF-induced expression of the potent vasoconstrictor ET-1 and its cognate ET-BR receptor occur via activation of HIF-1α, independent of hypoxia. PlGF levels are intrinsically elevated from the increased red cell turnover in SCD and in other chronic anemia (eg, thalassemia) and may contribute to inflammation and PHT seen in these diseases.

scholarly journals The role of endothelin-1 and the endothelin B receptor in the pathogenesis of hepatopulmonary syndrome in the rat

Hepatology ◽  
2004 ◽  
Vol 39 (6) ◽  
pp. 1593-1602 ◽  
Author(s):  
Yiqun Ling ◽  
Junlan Zhang ◽  
Bao Luo ◽  
Daisheng Song ◽  
Lichuan Liu ◽  
...  
Keyword(s):  
Hepatopulmonary Syndrome ◽  
Endothelin B Receptor ◽  
Endothelin 1 ◽  
Endothelin B

Autoregulation of endothelin-1 secretion by cultured human keratinocytes via the endothelin B receptor

1994 ◽  
Vol 1224 (3) ◽  
pp. 454-458 ◽  
Author(s):  
Joseph J. Yohn ◽  
Christopher Smith ◽  
Troy Stevens ◽  
Joseph G. Morelli ◽  
Libby R. Shurnas ◽  
...  
Keyword(s):  
Human Keratinocytes ◽  
Endothelin B Receptor ◽  
Endothelin 1 ◽  
Endothelin B
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