Comparative gene expression profiling of human umbilical vein endothelial cells and ocular vascular endothelial cells

Epidemiological studies have verified the critical role that antioxidative stress plays in protecting vascular endothelial cells. The aims of the present study were to investigate the antioxidative activities and differential regulation of nuclear erythroid-related factor 2- (Nrf2-) mediated gene expression by Xueshuan Xinmaining Tablet (XXT), a traditional Chinese medicine with the effect of treating cardiovascular diseases. The antioxidative activities of XXT were investigated using quantitative real-time PCR (qPCR), a PCR array, and western blotting. Our results indicated that XXT exhibited potent antioxidative activities by suppressing the levels of hydrogen peroxide- (H2O2-) induced reactive oxygen species (ROS) in human umbilical vein endothelial cells (HUVECs). We were also conscious of strong Nrf2-mediated antioxidant induction. XXT enhanced the expressions of Keap1, Nrf2, and Nrf2-mediated genes, such as glutamate-cysteine ligase modifier subunit (GCLM), NAD(P)H: quinine oxidoreductase 1 (NQO1), heme oxygenase 1 (HMOX1), and glutathione peroxidase (GPX) in HUVECs. In summary, XXT strongly activated Nrf2 and its downstream regulated genes, which may contribute to the antioxidative and vascular endothelial cell protective activities of XXT.

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Gene expression profiling to identify the toxicities and potentially relevant disease outcomes due to endosulfan exposure

Toxicology Research ◽

10.1039/c5tx00332f ◽

2016 ◽

Vol 5 (2) ◽

pp. 621-632 ◽

Cited By ~ 8

Author(s):

Dan Xu ◽

Shuai Li ◽

Limei Lin ◽

Fei Qi ◽

Xiaoming Hang ◽

...

Keyword(s):

Gene Expression ◽

Endothelial Cells ◽

Endothelial Dysfunction ◽

Gene Expression Profiling ◽

Expression Profiling ◽

Cellular Response ◽

Vascular Endothelial Cells ◽

Adverse Outcomes ◽

Vascular Endothelial ◽

Disease Outcomes

Endosulfan exposure induces gene expression shifts and affects cellular process in vascular endothelial cells. Adverse outcomes in cellular response result in endothelial dysfunction, associated with environmental diseases.

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Effect of prostaglandin E1 on TNF-induced vascular inflammation in human umbilical vein endothelial cells

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y10-028 ◽

2010 ◽

Vol 88 (5) ◽

pp. 576-583 ◽

Cited By ~ 14

Author(s):

Wentong Fang ◽

Hongjian Li ◽

Liaosheng Zhou ◽

Lequn Su ◽

Ying Liang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Endothelial Cells ◽

Cell Adhesion ◽

Adhesion Molecule ◽

Vascular Endothelial Cells ◽

Umbilical Vein ◽

Vascular Endothelial ◽

Oxygen Species ◽

Human Umbilical Vein ◽

Umbilical Vein Endothelial Cells

Prostaglandin E1 (PGE1) is a member of the prostaglandins and has a variety of cardiovascular protective effects. Increasing attention has been paid to the anti-inflammation activity of PGE1, but little direct evidence has been found. We investigated the effects of PGE1 on cell adhesion and inflammation and the mechanisms responsible for this activity in tumor necrosis factor (TNF)-treated human umbilical vein endothelial cells. Results demonstrated that pretreatment with PGE1 decreased the adhesion between vascular endothelial cells and monocytes, reduced the expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin in vascular endothelial cells. In addition, PGE1 suppressed TNF-induced NF-κB activation and production of reactive oxygen species. We concluded that PGE1 suppressed the vascular inflammatory process, which might be closely related to the inhibition of reactive oxygen species and NF-κB activation in human umbilical vein endothelial cells.

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miR-155 Promotes ox-LDL-Induced Autophagy in Human Umbilical Vein Endothelial Cells

Mediators of Inflammation ◽

10.1155/2017/9174801 ◽

2017 ◽

Vol 2017 ◽

pp. 1-7 ◽

Cited By ~ 11

Author(s):

Zhaozhi Zhang ◽

Xudong Pan ◽

Shaonan Yang ◽

Aijun Ma ◽

Kun Wang ◽

...

Keyword(s):

Endothelial Cells ◽

Vascular Endothelial Cells ◽

Umbilical Vein ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Vascular Endothelial ◽

Human Umbilical Vein ◽

Evolutionarily Conserved ◽

Autophagic Activity ◽

Umbilical Vein Endothelial Cells

As an evolutionarily conserved metabolic process, autophagy is involved in the process of atherosclerosis (AS). MicroRNA-155 (miR-155), a multifunctional miRNA, plays an important role in many physiological and pathological conditions, including AS and autophagy. However, the effect of miR-155 on the regulation of autophagy in endothelial cells has not been reported to date. Therefore, the objective of our study was to investigate the role of miR-155 in autophagy induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs). Our results demonstrated that ox-LDL induced autophagy in HUVECs and increased the expression of miR-155 significantly. Overexpression of miR-155 improved autophagic activity, whereas low expression of miR-155 inhibited autophagic activity. Therefore, the data demonstrated that miR-155 has a modulating effect on the autophagy of vascular endothelial cells.

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Genomic Survey of Cryptococcus neoformans-Induced Gene Expression Profiling in Human Brain Micro-Vascular Endothelial Cells

2007 Frontiers in the Convergence of Bioscience and Information Technologies ◽

10.1109/fbit.2007.68 ◽

2007 ◽

Author(s):

Ambrose Jong ◽

Chun-Hua Wu ◽

Wensheng Zhou ◽

Han-Min Chen ◽

Sheng-He Huang

Keyword(s):

Gene Expression ◽

Endothelial Cells ◽

Human Brain ◽

Gene Expression Profiling ◽

Cryptococcus Neoformans ◽

Expression Profiling ◽

Vascular Endothelial Cells ◽

Vascular Endothelial

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Interleukin-33 induces growth-regulated oncogene-α expression and secretion in human umbilical vein endothelial cells

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00435.2016 ◽

2017 ◽

Vol 313 (3) ◽

pp. R272-R279 ◽

Cited By ~ 4

Author(s):

Masayoshi Yamamoto ◽

Katsuyuki Umebashi ◽

Akinori Tokito ◽

Junichi Imamura ◽

Michihisa Jougasaki

Keyword(s):

Endothelial Cells ◽

Atherosclerotic Plaque ◽

Vascular Endothelial Cells ◽

Umbilical Vein ◽

Dependent Manner ◽

Vascular Endothelial ◽

Dot Blot ◽

Human Umbilical Vein ◽

Interleukin 33 ◽

Umbilical Vein Endothelial Cells

Although interleukin-33 (IL-33), a member of the IL-1 cytokine family, plays proinflammatory roles in immune cells as an “alarmin,” little is known regarding the biological actions of IL-33 on vascular endothelial cells. To investigate the effects of IL-33 on vascular endothelial cells, we first screened the IL-33-regulated proteins in human umbilical vein endothelial cells (HUVECs) using a dot blot array and observed that IL-33 markedly increased growth-regulated oncogene-α (GRO-α), a chemokine that is also known as chemokine (C-X-C motif) ligand 1 (CXCL1). Real-time reverse transcription PCR and ELISA demonstrated that IL-33 induced GRO-α expression and secretion in HUVECs in a dose- and a time-dependent manner. Western immunoblot assay revealed that IL-33 activated the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun NH2 -terminal kinase (JNK). In addition, translocation of nuclear factor-κB (NF-κB) p65 to the nucleus of HUVECs was observed by IL-33 stimulation. Furthermore, treatment with pharmacological inhibitors against ERK1/2 (PD98059), JNK (SP600125), or NF-κB (BAY11-7085) significantly suppressed IL-33-induced GRO-α gene expression and secretion from HUVECs. Moreover, immunohistochemical staining demonstrated that IL-33 and GRO-α coexpressed in the endothelium of human carotid atherosclerotic plaque. Taken together, the present study indicates that IL-33 localized in the human atherosclerotic plaque increases GRO-α mRNA expression and protein secretion via activation of ERK1/2, JNK, and NF-κB in HUVECs, suggesting that IL-33 plays an important role in the pathophysiology and development of atherosclerosis.

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