scholarly journals Angiotensin II Impairs Endothelial Progenitor Cell Number and Function In Vitro and In Vivo

Hypertension ◽  
2011 ◽  
Vol 58 (3) ◽  
pp. 394-403 ◽  
Author(s):  
Cathleen Endtmann ◽  
Talin Ebrahimian ◽  
Thomas Czech ◽  
Omar Arfa ◽  
Ulrich Laufs ◽  
...  
2009 ◽  
Vol 117 (10) ◽  
pp. 355-364 ◽  
Author(s):  
Gian Paolo Fadini ◽  
Mattia Albiero ◽  
Andrea Cignarella ◽  
Chiara Bolego ◽  
Christian Pinna ◽  
...  

The beneficial or detrimental effects of androgens on the cardiovascular system are debated. Endothelial progenitor cells are bone-marrow-derived cells involved in endothelial healing and angiogenesis, which promote cardiovascular health. Oestrogens are potent stimulators of endothelial progenitor cells, and previous findings have indicated that androgens may improve the biology of these cells as well. In the present study, we show that testosterone and its active metabolite dihydrotestosterone exert no effects on the expansion and function of late endothelial progenitors isolated from the peripheral blood of healthy human adult males, whereas they positively modulate early ‘monocytic’ endothelial progenitor cells. In parallel, we show that castration in rats is followed by a decrease in circulating endothelial progenitor cells, but that testosterone and dihydrotestosterone replacement fails to restore endothelial progenitor cells towards normal levels. This is associated with persistently low oestrogen levels after androgen replacement in castrated rats. In a sample of 62 healthy middle-aged men, we show that circulating endothelial progenitor cell levels are more directly associated with oestradiol, rather than with testosterone, concentrations. In conclusion, our results collectively demonstrate that androgens exert no direct effects on endothelial progenitor cell biology in vitro and in vivo.


FEBS Letters ◽  
2008 ◽  
Vol 582 (11) ◽  
pp. 1607-1612 ◽  
Author(s):  
Rei Shibata ◽  
Carsten Skurk ◽  
Noriyuki Ouchi ◽  
Gennaro Galasso ◽  
Kazuhisa Kondo ◽  
...  

2019 ◽  
Vol 52 ◽  
pp. 537-544 ◽  
Author(s):  
Hsiang-Ping Lee ◽  
Po-Chun Chen ◽  
Shih-Wei Wang ◽  
Yi-Chin Fong ◽  
Chang-Hai Tsai ◽  
...  

2013 ◽  
Vol 228 (1) ◽  
pp. 94-97 ◽  
Author(s):  
Sridevi Devaraj ◽  
Alexander Chien ◽  
Bhavana Rao ◽  
Xinpu Chen ◽  
Ishwarlal Jialal

2009 ◽  
Vol 104 (10) ◽  
pp. 2500-2507 ◽  
Author(s):  
Andrea Garolla ◽  
Renata D’Incà ◽  
Davide Checchin ◽  
Andrea Biagioli ◽  
Luca De Toni ◽  
...  

2018 ◽  
Vol 12 (7) ◽  
pp. 1594-1607 ◽  
Author(s):  
Sheetal Kadam ◽  
Meghana Kanitkar ◽  
Kadambari Dixit ◽  
Rucha Deshpande ◽  
Vasudevan Seshadri ◽  
...  

Blood ◽  
2011 ◽  
Vol 118 (13) ◽  
pp. 3743-3755 ◽  
Author(s):  
Francesca Margheri ◽  
Anastasia Chillà ◽  
Anna Laurenzana ◽  
Simona Serratì ◽  
Benedetta Mazzanti ◽  
...  

Abstract Endothelial urokinase-type plasminogen activator receptor (uPAR) is thought to provide a regulatory mechanism in angiogenesis. Here we studied the proangiogenic role of uPAR in endothelial colony-forming cells (ECFCs), a cell population identified in human umbilical blood that embodies all of the properties of an endothelial progenitor cell matched with a high proliferative rate. By using caveolae-disrupting agents and by caveolin-1 silencing, we have shown that the angiogenic properties of ECFCs depend on caveolae integrity and on the presence of full-length uPAR in such specialized membrane invaginations. Inhibition of uPAR expression by antisense oligonucleotides promoted caveolae disruption, suggesting that uPAR is an inducer of caveolae organization. Vascular endothelial growth factor (VEGF) promoted accumulation of uPAR in ECFC caveolae in its undegraded form. We also demonstrated that VEGF-dependent ERK phosphorylation required integrity of caveolae as well as caveolar uPAR expression. VEGF activity depends on inhibition of ECFC MMP12 production, which results in impairment of MMP12-dependent uPAR truncation. Further, MMP12 overexpression in ECFC inhibited vascularization in vitro and in vivo. Our data suggest that intratumor homing of ECFCs suitably engineered to overexpress MMP12 could have the chance to control uPAR-dependent activities required for tumor angiogenesis and malignant cells spreading.


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