The neuropeptide galanin promotes an anti-thrombotic phenotype on endocardial endothelial cells from heart failure patients

2017 ◽  
Vol 206 ◽  
pp. 35-42 ◽  
Author(s):  
Christina Tyrrell ◽  
Amanda Toyooka ◽  
Faiza Khan ◽  
Kent L. Thornburg ◽  
James O. Mudd ◽  
...  
2008 ◽  
Vol 104 (3) ◽  
pp. 307-320 ◽  
Author(s):  
Giampiero Rocca ◽  
Antonino Stefano ◽  
Ermanno Eleuteri ◽  
Rita Anzalone ◽  
Francesca Magno ◽  
...  

2017 ◽  
Vol 95 (10) ◽  
pp. 1224-1229 ◽  
Author(s):  
Danielle Jacques ◽  
Pedro D’Orléans-Juste ◽  
Sheldon Magder ◽  
Ghassan Bkaily

Endocardial endothelial cells (EECs) constitute an important component of the heart. These cells form a monolayer that covers the cavities of the right (EECRs) and left (EECLs) ventricles. They play an important role in cardiac excitation–contraction coupling via their secretion of cardioactive factors such as neuropeptide Y (NPY). They also contribute to cardiac pathology such as arrhythmia, hypertrophy, and heart failure. Differences between EECRs and EECLs contribute to tuning of circulating factors at the entry and exit of the ventricles. NPY, via activation of its receptors, modulates the excitation–secretion coupling of EECs, thus, indirectly modulating cardiac function and remodeling.


2015 ◽  
Vol 230 (8) ◽  
pp. 1964-1973 ◽  
Author(s):  
Quanlu Duan ◽  
Lei Yang ◽  
Wei Gong ◽  
Sandip chaugai ◽  
Feng Wang ◽  
...  

2016 ◽  
Vol 231 (12) ◽  
pp. 2700-2710 ◽  
Author(s):  
Micaela Pannella ◽  
Cristiana Caliceti ◽  
Francesca Fortini ◽  
Giorgio Aquila ◽  
Francesco Vieceli Dalla Sega ◽  
...  

2011 ◽  
Vol 31 (2) ◽  
pp. 75-82 ◽  
Author(s):  
Vicenta Martínez-Sales ◽  
Ignacio Sánchez-Lázaro ◽  
Virtudes Vila ◽  
Luis Almenar ◽  
Teresa Contreras ◽  
...  

Introduction and Aims:Acute and chronic heart failure may manifest different degrees of endothelial damage and angiogenesis. Circulating endothelial cells (CEC) have been identified as marker of vascular damage. The aim of our study was to evaluate the evolution of the CEC at different stages of patients with heart failure. We also investigated a potential correlation between CEC and markers of vascular damage and angiogenesis.Methods:We studied 32 heart failure patients at hospital admission (acute phase) and at revision after 3 months (stable phase) and 32 controls. Circulating markers of endothelial damage (CEC; von Willebrand factor, vWF and soluble E-selectin, sEsel) and angiogenesis (vascular endothelial growth factor, VEGF and thrombospondin-1) were quantified.Results:Levels of CEC, vWF, sEsel and VEGF are significantly higher in heart failure patients than in controls. Levels of CEC (36.9 ± 15.3 vs. 21.5 ± 10.0 cells/ml;p< 0.001), vWF (325 ± 101 vs. 231 ± 82%;p< 0.001) and VEGF (26.3 ± 15.2 vs. 21.9 ± 11.9 ng/ml;p< 0.001) are significantly higher in the acute phase than in the stable phase of heart failure. CEC levels correlate with vWF and VEGF. Results show than 100% of patients in acute phase and 37.5% in stable phase have levels of CEC higher than the 99th percentile of the distribution of controls (16 cells/ml). Therefore, increases in CEC represent a relative risk of 9.5 for heart failure patients suffering from acute phase.Conclusions:CEC, in addition to being elevated in heart failure, correlate with vWF levels, providing further support for CEC as markers of endothelial damage. Levels of CEC are associated with the acute phase of heart failure and could be used as a marker of the worsening in heart failure.


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