subendothelial

subendothelial

 [sub″en-do-the´le-al]
beneath an endothelial layer.

sub·en·do·the·li·al

(sŭb'en-dō-thē'lē-ăl),
Below the endothelium.

subendothelial

/sub·en·do·the·li·al/ (-the´le-al) beneath the endothelium.

subendothelial

beneath an endothelial layer.

subendothelial coat
a layer of connective tissue and fibroblasts beneath the endothelium of blood vessels and the heart.
subendothelial space
potential connective tissue space beneath the endothelium of blood vessels and the heart.
References in periodicals archive ?
Further, oxidized LDL is capable of stimulating endothelial cells to express adhesion molecules, which attract excess of foamy macrophages under the subendothelial layer, thereby promoting the seeding process of plaque formation.
Primary hemostasis is defined as the platelet-vessel wall interaction at the site of vascular injury that initiates when flowing platelets recognize (through their receptors) and bind (through the adhesive protein von Willebrand factor) subendothelial collagen.
So this endothelial dysfunction, fueled by high oxidative stress secondary to insulin resistance, oxidizes LDL that in turn is targeted by monocytes that then migrate into the subendothelial space, stimulating macrophages to form foam cells.
Upon deposition in the vascular wall, MPO is preferentially situated in the subendothelial matrix (Baldus et al.
The common inflammatory process affecting multiple organ systems in HSP is that of leukocytoclastic vasculitis triggered by subendothelial deposition of circulating IgA immune complexes in small arteries and capillaries.
Immunohistochemical studies showed CD31 and CD34 positive cells lining the blood vessels, and subendothelial layer appeared cells positive for smooth muscle actin [Figure 1]e-[Figure 1]g.
Endothelial adhesion molecules specifically and strongly bind to monocytes and lymphocytes of the blood, that is the basis for subsequent differential migration of these cells in the subendothelial space of the vessel, induced by specific factors (TNF-[alpha], monocyte chemoattractant protein (MCP-1)).
Tumor cell retention in target organs maybe due to size restriction, or it maybe the consequence of selective molecular adhesive interactions with microvascular endothelial cells or the subendothelial basement membrane.
Macrophages play a key role in atherogenesis by releasing proinflammatory cytokines and forming foam cells in subendothelial lesions.