Endothelial cell loss after phacoemulsification: relation to preoperative and intraoperative parameters.
The role of miR-19b in the inhibition of
endothelial cell apoptosis and its relationship with coronary artery disease.
Specular microscopy and confocal microscopy are employed for morphological and morphometric evaluation of
endothelial cells in vivo (CANAVAGH et al., 2000; ABIB et al., 2012; NAGATSUYU et al., 2014; BERCHT et al., 2015).
The mean value of Corneal
Endothelial Cell Density (ECD) was 2021.548 +- 528.142 cells/mm2 in PXS patients and the mean value of ECD in healthy subjects was 2772.692 +- 383.395 cells/mm2 with statistically significant (p-value <0.05) difference between both groups showing that the patients with PXS had significantly lower ECD in comparison to healthy controls.
Continued
endothelial cell loss ten years after lens implantation.
Experimental studies have demonstrated a relationship between elevated IOP and
endothelial cell loss in animal models, and a clinical study in glaucoma patients with healthy corneas showed that the patients had a significantly lower ECD compared with a control group with normal IOP [54, 55].
In vitro models of
endothelial cells from lung tissue are important tools for understanding the interactions between the endothelium and leukocyte trafficking [16].
Most frequent macrophages and macrophage-derived cells showed TNFalpha positivity (14 cases, 43.74% showed TNFalpha faint positivity in macrophages and 12 cases of 17, 70.58% showed similar positivity in multinucleated giant cells); less numerous cases had mesenchymal cells positivity (15 cases, 46.875%) and
endothelial cells positivity (8 cases, 25.00%) (Figure 2(f)).
The data in this study imply that leptin/LEPR interaction stimulated IL-8 production in
endothelial cells, consequently promoting neutrophil chemotaxis and PE progression.
E-selectin expression is found only on
endothelial cells after activation of proinflammatory cytokines (interleukin-1, tumor necrosis factor) or endotoxin.
Moreover, reduced levels of Kallikreins 9,11, and 12, three serine proteases with angiogenic activity, have been observed in SSc
endothelial cell [41, 42].
Hyperglycemia impairs autophagy in HUVECs through inhibition of the phosphorylation of AMPK, activating the downstream effector mTOR through mTOR phosphorylation and leading to
endothelial cell damage.
