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2015 ; 10
(7
): e0127931
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Nitric Oxide Increases Arterial Endotheial Permeability through Mediating
VE-Cadherin Expression during Arteriogenesis
#MMPMID26133549
Yang B
; Cai B
; Deng P
; Wu X
; Guan Y
; Zhang B
; Cai W
; Schaper J
; Schaper W
PLoS One
2015[]; 10
(7
): e0127931
PMID26133549
show ga
Macrophage invasion is an important event during arteriogenesis, but the
underlying mechanism is still only partially understood. The present study tested
the hypothesis that nitric oxide (NO) and VE-cadherin, two key mediators for
vascular permeability, contribute to this event in a rat ischemic hindlimb model.
In addition, the effect of NO on expression of VE-caherin and endothelial
permeability was also studied in cultured HUVECs. We found that: 1) in normal
arteriolar vessels (NAV), eNOS was moderately expressed in endothelial cells (EC)
and iNOS was rarely detected. In contrast, in collateral vessels (CVs) induced by
simple femoral artery ligation, both eNOS and iNOS were significantly upregulated
(P<0.05). Induced iNOS was found mainly in smooth muscle cells, but also in other
vascular cells and macrophages; 2) in NAV VE-cadherin was strongly expressed in
EC. In CVs, VE-cadherin was significantly downregulated, with a discontinuous and
punctate pattern. Administration of nitric oxide donor DETA NONOate (NONOate)
further reduced the amounts of Ve-cadherin in CVs, whereas NO synthase inhibitor
L-NAME inhibited downregulation of VE-cadherin in CVs; 3) in normal rats Evans
blue extravasation (EBE) was low in the musculus gracilis, FITC-dextron leakage
was not detected in the vascular wall and few macrophages were observed in
perivascular space. In contrast, EBE was significantly increased in femoral
artery ligation rats, FITC-dextron leakage and increased amounts of macrophages
were detected in CVs, which were further enhanced by administration of NONOate,
but inhibited by L-NAME supplement; 4) in vitro experiments confirmed that an
increase in NO production reduced VE-cadherin expression, correlated with
increases in the permeability of HUVECs. In conclusion, our data for the first
time reveal the expression profile of VE-cadherin and alterations of vascular
permeability in CVs, suggesting that NO-mediated VE-cadherin pathway may be one
important mechanism responsible, at least in part, for macrophage invasion during
arteriogenesis.
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