Endothelial cells

Influence of cyclophilin D protein expression level on endothelial cell oxidative damage resistance

J. Z. Peng, Xue, L., Chen, J., Chen, B. S., and Yang, Y. Q., Influence of cyclophilin D protein expression level on endothelial cell oxidative damage resistance, vol. 14, pp. 4258-4268, 2015.

We examined the influence of cyclophilin-D (CypD) protein expression level on endothelial cell oxidative damage resistance. A model of CypD protein expression or high expression in endothelial cells was established through gene silencing or cloning. The comparable groups were normal endothelial cells cultured in phosphate-buffered solution in liquid handling cells containing 500 mM H2O2 for 90 or 120 min, and then the medium was replaced with common nutrient solution and cultured again for 24 h.

Protective effects of hydrogen-rich medium on lipopolysaccharide-induced monocytic adhesion and vascular endothelial permeability through regulation of vascular endothelial cadherin

Y. Yu, Wang, W. N., Han, H. Z., Xie, K. L., Wang, G. L., and Yu, Y. H., Protective effects of hydrogen-rich medium on lipopolysaccharide-induced monocytic adhesion and vascular endothelial permeability through regulation of vascular endothelial cadherin, vol. 14, pp. 6202-6212, 2015.

We observed the effect of hydrogen-rich medium on lipopolysaccharide (LPS)-induced human umbilical vein endothelial cells (HUVECs), hyaline leukocyte conglutination, and permeability of the endothelium. Endotheliocytes were inoculated on 6-well plates and randomly divided into 4 groups: control, H2, LPS, LPS+H2, H2, and LPS+H2 in saturated hydrogen-rich medium.

Endothelial cells on the proliferation and expression of intercellular adhesion molecule 1 and interleukin 8 of vascular smooth muscle cells

H. - P. Tang, Sun, L. - X., and Han, W., Endothelial cells on the proliferation and expression of intercellular adhesion molecule 1 and interleukin 8 of vascular smooth muscle cells, vol. 12, pp. 4363-4370, 2013.

The aim of this study was to investigate the influence of activated endothelial cells on the proliferation and secretion of vas­cular smooth muscle cells (VSMCs). Cultured lung microvascular endothelial cells were treated with or without tumor necrosis factor alpha (TNF-α; 10 ng/mL) for 6 h, and the supernatant was collected and filtered. The supernatant with TNF-α was called fluid A, and that without TNF-α was called fluid B.

RXR agonists inhibit high glucose-induced upregulation of inflammation by suppressing activation of the NADPH oxidase-nuclear factor-κB pathway in human endothelial cells

R. B. Ning, Zhu, J., Chai, D. J., Xu, C. S., Xie, H., Lin, X. Y., Zeng, J. Z., and Lin, J. X., RXR agonists inhibit high glucose-induced upregulation of inflammation by suppressing activation of the NADPH oxidase-nuclear factor-κB pathway in human endothelial cells, vol. 12, pp. 6692-6707, 2013.

An inflammatory response induced by high glucose is a cause of endothelial dysfunction in diabetes and is an important contributing link to atherosclerosis. Diabetes is an independent risk factor of atherosclerosis and activation of retinoid X receptor (RXR) has been shown to exert anti-atherogenic effects. In the present study, we examined the effects of the RXR ligands 9-cis-retinoic acid (9-cis-RA) and SR11237 on high glucose-induced inflammation in human umbilical endothelial vein endothelial cells (HUVECs) and explored the potential mechanism.

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