endothelial cell

(redirected from endotheliocyte)
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endothelial cell

[‚en·də¦thē·lē·əl ′sel]
(histology)
A type of squamous epithelial cell composing the endothelium.
References in periodicals archive ?
In addition, coagulation factors are activated after the interaction of platelets and endotheliocyte, thus enhancing coagulation and inflammation [56].
This was revealed first of all through the emergence of numerous micropinocytotic vesicles in luminal locuses of endotheliocyte cytoplasm in blood capillaries of bone marrow.
Scanning electronic microscopy showed decrease in number and sizes of micro-erosion on the apical surface of endotheliocyte. The restoration of the closed adhesion of the epithelial cells to each other and decrease in number of inclusions on the lumen surface were found too (Figure 6).
At the same time, TNF-a can activate the NF-kB in hepatocytes, Kupffer cells and endotheliocyte, which increases expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and selectin, and these inflammatory factors further impel the inflammatory injury of hepatocytes (Issekutz 1990; Essanietal.
Song et al., "Evaluation of miR-29c inhibits endotheliocyte migration and angiogenesis of human endothelial cells by suppressing the insulin like growth factor 1," American Journal of Translational Research, vol.
Flow cytometry analysis of ADSC at passages 34 demonstrated that the cells were negative for leukocyte and endotheliocyte markers, CD45 (1.71%) and CD31 (0.21%), and positive for mesenchymal stem cell markers, CD44 (98.4%) and CD90 (99.9%) (Figure 1(d)).
Human postnatal dental pulp cells co-differentiate into osteoblasts and endotheliocytes: a pivotal synergy leading to adult bone tissue formation.
Carmona et al .'s findings[41] confirmed that indoxyl sulfate is associated with the poor prognosis of chronic kidney disease and cardiovascular disease owing to the injury of endotheliocytes, and that it is able to promote the formation of endothelial vesicles with varying molecules that maintain the homeostasis of EPCs.
Sampaolesi et al., "Human postnatal dental pulp cells co-differentiate into osteoblasts and endotheliocytes: a pivotal synergy leading to adult bone tissue formation," Cell Death and Differentiation, vol.
There are several lines of evidence indicating that the ET-1-induced endothelial dysfunction is realized through decreasing production and increasing degradation of NO, through enhancement of Von Willebrand factor and reactive oxygen species formation, and also through the activation of proinflammatory metabolic pathways in the endotheliocytes [4].