Enhanced platelet adhesiveness to the subendothelium
and higher protein exudation through vessel wall may promote atherosclerotic tendency.
The human umbilical cord is a promising source of MSCs, as MSCs can be isolated either from the whole umbilical cord [16,77], the umbilical vein subendothelium
, or WJ [14, 19, 74].
Macrophages stimulated by the treatment of nicotine secrete elevated inflammatory cytokines, namely, tumor necrosis factor-[alpha] (TNF-[alpha]), IL-1[beta], and chemokines, creating the proinflammatory microenvironment in the subendothelium
Gut microbe-derived TMAO could enforce the expression of the receptor of SR-A and CD36, which promotes the formation of foam cells whose accumulation within the subendothelium
or neointima constitutes the first step in AS.
Pathologic diagnosis was based on the presence of all 3 of the following histologic signs: widening of subendothelium
with myxoid degeneration, intraluminal thrombus formation, and fibrinoid necrosis of terminal arterioles.
The longer retention of sdLDL in subendothelium
makes easier their modification by oxidation or the glycation, so their role in the development of endothelial dysfunction is usually attributed to oxidative modification and to the mechanisms of action of oxidised LDL (oxLDL) .
Increased TG induces thrombosis associated with neutrophil adhesion during the inflammatory response initiated when injury to a vessel wall exposes the blood to tissue factor in the subendothelium
(Rau et al., 2007).
The other possible mechanisms are chemical arteritis and tissue destruction of endothelium, subendothelium
, or muscle layers of vessel (1, 6, 7).
Morphological studies revealed that endothelium and subendothelium
containing collagen fibers covered the graft completely and neointima was formed.
This interaction plays a key role in the initial adhesion of platelets to the subendothelium
, which in turn induces a complex cascade of signals which results in platelet aggregation .
(22) Anemia could further worsen the bleeding disorder because red cells release ADP and facilitate platelets contacting with subendothelium
at the damage site.
Migration of monocytes into the subendothelium
is the initial step of inflammation and atherosclerotic plaque formation, which plays a key role in the atherosclerotic plaque formation.