Biomedical Engineering Reference
In-Depth Information
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Fig. 4
Schema depicting the mechanisms by which apoC-III induces monocyte adhesion to
vascular EC via activation of cellular adhesion molecules. ApoC-III, alone or as a component of
circulating apoB lipoproteins, recognized by TLR-2, activates NF-κB through MyD88-dependent
pathway, resulting in increased monocyte expression of β1-integrin (Kawakami
et al.
2008b).
PKCα activation, through PC-PLC, participates in apoC-III-induced β1-integrin activation via
NF-κB (Kawakami
et al.
2006a, 2007), and RhoA may also be involved (Kawakami
et al.
2006a).
In vascular endothelial cells, apoC-III induces VCAM-1 and ICAM-1 expression via PKCβ-
mediated activation of NF-κB (Kawakami
et al.
2006b). Induction of monocyte β1-integrin and
endothelial cell VCAM-1 and ICAM-1 by apoC-III enhances monocyte adhesion under static
and l ow conditions. VCAM-1, vascular cell adhesion molecule 1; ICAM-1, intercellular adhesion
molecule 1; NF- κB, nuclear factor κB; PKC, protein kinase C; TLR2, toll-like receptor 2; MyD88,
myeloid dif erentiation primary response gene 88.
ApoC-III Induces Monocyte Adhesion to Vascular EC under
Static and Flow Conditions
h e adhesion of circulating monocytes to vascular endothelium
contributes
importantly to the inl ammatory aspects of atherogenesis (Libby 2002, Libby and
Aikawa 2002).
Monocytes from hypercholesterolemic patients have increased
expression of integrins and other adhesion molecules and
show increased adhesion
to EC
in vitro
. In this study we hypothesized that apoB lipoproteins
with apoC-III
could induce monocyte activation and subsequent adhesion
to EC.
We isolated apoC-III containing VLDL and LDL lipoproteins from plasma of
healthy volunteers by immunoai nity chromatography and ultracentrifugation.
