scholarly journals Zoledronate induces autophagic cell death in human umbilical vein endothelial cells via Beclin-1 dependent pathway activation

2016 ◽  
Vol 14 (5) ◽  
pp. 4747-4754 ◽  
Author(s):  
Yong Lu ◽  
Zhiyong Wang ◽  
Wei Han ◽  
Hao Li
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Umbilical Vein ◽  
Autophagic Cell Death ◽  
Beclin 1 ◽  
Human Umbilical Vein ◽  
Pathway Activation ◽  
Umbilical Vein Endothelial Cells ◽  
Dependent Pathway

Lipid mediators of autophagy in stress-induced premature senescence of endothelial cells

2008 ◽  
Vol 294 (3) ◽  
pp. H1119-H1129 ◽  
Author(s):  
Susann Patschan ◽  
Jun Chen ◽  
Alla Polotskaia ◽  
Natalja Mendelev ◽  
Jennifer Cheng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Umbilical Vein ◽  
Acid Sphingomyelinase ◽  
Premature Senescence ◽  
Human Umbilical Vein ◽  
Glycation End Products ◽  
Umbilical Vein Endothelial Cells ◽  
Stress Induced Premature Senescence

Our group (Patschan S, Chen J, Gealekman O, Krupincza K, Wang M, Shu L, Shayman JA, Goligorsky MS; Am J Physiol Renal Physiol 294: F100–F109, 2008) previously observed an accumulation of gangliosides coincident with development of cell senescence and demonstrated lysosomal permeabilization in human umbilical vein endothelial cells exposed to glycated collagen I (GC). Therefore, we investigated whether the lysosome-dependent, caspase-independent or type 2-programmed cell death (autophagy) is involved in development of premature senescence of endothelial cells. The cleaved microtubule-associated protein 1 light-chain 3 (LC3), a marker of autophagosome formation, was overexpressed within 24 h of GC treatment; however, by 4–5 days, it was nearly undetectable. Early induction of autophagosomes was associated with their fusion with lysosomes, a phenomenon that later became subverted. Autophagic cell death can be triggered by the products of damaged plasma membrane, sphingolipids, and ceramide. We observed a clustering of membrane rafts shortly after exposure to GC; later, after 24 h, we observed an internalization, accompanied by an increased acid sphingomyelinase activity and accumulation of ceramide. Pharmacological inhibition of autophagy prevented development of premature senescence but did lead to the enhanced rate of apoptosis in human umbilical vein endothelial cells exposed to GC. Pharmacological induction of autophagy resulted in reciprocal changes. These observations appear to represent a mechanistic molecular cascade whereby advanced glycation end products like GC induce sphingomyelinase activity, accumulation of ceramide, clustering, and later internalization of lipid rafts.

scholarly journals Curcumin Protects Human Umbilical Vein Endothelial Cells against H2O2-Induced Cell Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Jipeng Ouyang ◽  
Rong Li ◽  
Haiqin Shi ◽  
Jianping Zhong
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Death ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Therapeutic Drug ◽  
Human Umbilical Vein ◽  
Antioxidative Enzyme Activities ◽  
Apoptosis Related Protein ◽  
Umbilical Vein Endothelial Cells

Migraine is a prevalent neurological disorder which causes a huge economic burden on society. It is thought to be a neurovascular disease with oxidative stress might be involved. Curcumin, one of the major ingredients of turmeric, has potent antioxidative and anti-inflammatory properties, but whether it could be used as a potential treatment for migraine remains to be explored. In the present study, human umbilical vein endothelial cells (HUVECs) were pretreated with various concentrations of curcumin (0 μM, 10 μM, 20 μM, 30 μM, 40 μM, and 50 μM) for 12 h, thereby exposed to H2O2 (100 μM) for another 12 h. The viability of HUVECs was tested by the CCK-8 assay, and the activities of antioxidant enzymes including superoxide dismutase (SOD) and glutathione (GSH) were also examined. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were assayed to determine H2O2-induced oxidative stress. In addition, several cell death-related genes (p53, p21, Bax, and Bcl-2) were detected by PCR, and an apoptosis-related protein (caspase3) was evaluated by western blotting. Our results showed that curcumin improved the H2O2-induced decrease of cell viability and antioxidative enzyme activities and decreased the level of oxidative stress. As a conclusion, curcumin could mitigate H2O2-induced oxidative stress and cell death in HUVECs and may be a potential therapeutic drug for migraine.

Effect of flupirtine on cell death of human umbilical vein endothelial cells induced by reactive oxygen species

1998 ◽  
Vol 56 (12) ◽  
pp. 1615-1624 ◽  
Author(s):  
Bernd Lorenz ◽  
Thomas Schlüter ◽  
Ralf Bohnensack ◽  
Gabriela Pergande ◽  
Werner E.G Müller
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Cell Death ◽  
Umbilical Vein ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals Long-Zhi Decoction Medicated Serum Promotes Angiogenesis in Human Umbilical Vein Endothelial Cells Based on Autophagy

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Quan He ◽  
Qihua Liu ◽  
Yongbin Chen ◽  
Jiaquan Meng ◽  
Ling Zou
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Diseases ◽  
The Elderly ◽  
Tube Formation ◽  
Beclin 1 ◽  
Effective Response ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Ischemic stroke (IS) is a fatal subtype of stroke that lacks effective treatments. Angiogenesis following IS is an effective response that mediates brain recovery and repair. Our previous study demonstrated that long-zhi decoction (LZD), a Chinese herbal formula, promoted angiogenesis in rats of IS model. To further investigate the association between the proangiogenic mechanism of an LZD-medicated serum and cellular autophagy, we evaluated its promotional effect on angiogenesis in human umbilical vein endothelial cells (HUVECs) in vitro. We used HUVECs subjected to H2O2 to induce injury and observed the effects of the LZD-medicated serum treatment. Cell-based assays included proliferation, migration, and tube formation. To assess the extent of autophagy, transmission electron microscopy was used to measure the number of autophagosomes. Immunofluorescence and Western blotting were performed to evaluate the autophagy-related protein of LC3-II and Beclin-1. The LZD-medicated serum promoted proliferation, migration, and tube formation in HUVECs. The LZD-medicated serum also increased the autophagosomes and the autophagic protein expressions of LC3-II and Beclin-1. The proangiogenic and autophagic activity of LZD provides new cogitations to its clinical application and may lead to potential drug development for treating various vascular diseases, especially in the elderly, in the future.

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