Biomedical Engineering Reference
In-Depth Information
control
control
antibody to VCAM-1
antibody to ICAM-1
antibodies to VCAM-1 & ICAM-1
non-specific IgG
antibody to VCAM-1
antibody to ICAM-1
antibodies to VCAM-1 & ICAM-1
non-specific IgG
9
9
**
**
*
*
*
*
8
8
7
7
#
#
6
6
5
5
##
##
4
4
#
#
#
#
3
3
2
2
1
1
0
0
Vehicle
Vehicle
cLDL
cLDL
nLDL
nLDL
Fig. 5
Inhibition of monocyte adhesion by antibody to ICAM-1 or VCAM-1. HCAECs were
treated with 200 μg/mL cLDL for 16 hr in 96-well plates. Control cells were treated with either
vehicle or 200 μg/mL nLDL. Anti-ICAM-1, anti-VCAM-1 or both antibodies were added to
HCAECs 2 hr prior to the application of labeled monocytes (i nal concentration of 10 ng/mL).
Non-specii c IgGs served as antibody treatment control. n = 3-4 per point, *P < 0.05, **P < 0.01
vs. vehicle control cells pretreated with the same antibody,
#
P < 0.05,
##
P < 0.001 vs. no antibody
control cells (white bars) subjected to the same treatment. Permission to publish obtained from
Wolters Kluwer Health.
h e control siRNA did not protect the endothelial cells from monocyte adhesion.
h ese experiments provided evidence that ICAM-1 in cooperation with VCAM-1
is involved in monocyte adhesion by cLDL-activated human endothelial cells
in vitro
.
APPLICATIONS TO OTHER AREAS OF HEALTH AND
DISEASE
Because urea is present in normal plasma, these observations may be applicable
not only to renal patients but also to healthy individuals. While our data were
obtained mainly using ESRD patients, the role of cLDL in atherosclerosis is
certainly applicable to early stages of CKD, which includes more than 20 million
adults in the United States and many more around the world.
