scholarly journals Different RNA splicing mechanisms contribute to diverse infective outcome of classical swine fever viruses of differing virulence: insights from the deep sequencing data in swine umbilical vein endothelial cells

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2113 ◽  
Author(s):  
Pengbo Ning ◽  
Yulu Zhou ◽  
Wulong Liang ◽  
Yanming Zhang
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Rna Splicing ◽  
Molecular Mechanisms ◽  
Computational Study ◽  
Umbilical Vein ◽  
Classical Swine Fever ◽  
Pathway Enrichment Analysis ◽  
Splicing Regulation ◽  
Umbilical Vein Endothelial Cells

Molecular mechanisms underlying RNA splicing regulation in response to viral infection are poorly understood. Classical swine fever (CSF), one of the most economically important and highly contagious swine diseases worldwide, is caused by classical swine fever virus (CSFV). Here, we used high-throughput sequencing to obtain the digital gene expression (DGE) profile in swine umbilical vein endothelial cells (SUVEC) to identify different response genes for CSFV by using both Shimen and C strains. The numbers of clean tags obtained from the libraries of the control and both CSFV-infected libraries were 3,473,370, 3,498,355, and 3,327,493 respectively. In the comparison among the control, CSFV-C, and CSFV-Shimen groups, 644, 158, and 677 differentially expressed genes (DEGs) were confirmed in the three groups. Pathway enrichment analysis showed that many of these DEGs were enriched in spliceosome, ribosome, proteasome, ubiquitin-mediated proteolysis, cell cycle, focal adhesion, Wnt signalling pathway, etc., where the processes differ between CSFV strains of differing virulence. To further elucidate important mechanisms related to the differential infection by the CSFV Shimen and C strains, we identified four possible profiles to assess the significantly expressed genes only by CSFV Shimen or CSFV C strain. GO analysis showed that infection with CSFV Shimen and C strains disturbed ‘RNA splicing’ of SUVEC, resulting in differential ‘gene expression’ in SUVEC. Mammalian target of rapamycin (mTOR) was identified as a significant response regulator contributed to impact on SUVEC function for CSFV Shimen. This computational study suggests that CSFV of differing virulence could induce alterations in RNA splicing regulation in the host cell to change cell metabolism, resulting in acute haemorrhage and pathological damage or infectious tolerance.

scholarly journals Dengue Virus Induces Novel Changes in Gene Expression of Human Umbilical Vein Endothelial Cells

2003 ◽  
Vol 77 (21) ◽  
pp. 11822-11832 ◽  
Author(s):  
Rajas V. Warke ◽  
Kris Xhaja ◽  
Katherine J. Martin ◽  
Marcia F. Fournier ◽  
Sunil K. Shaw ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Dengue Virus ◽  
Immune Cell ◽  
Umbilical Vein ◽  
Oligoadenylate Synthetase ◽  
Functional Responses ◽  
Human Umbilical Vein ◽  
Phospholipid Scramblase ◽  
Umbilical Vein Endothelial Cells

ABSTRACT Endothelial cells are permissive to dengue virus (DV) infection in vitro, although their importance as targets of DV infection in vivo remains a subject of debate. To analyze the virus-host interaction, we studied the effect of DV infection on gene expression in human umbilical vein endothelial cells (HUVECs) by using differential display reverse transcription-PCR (DD-RTPCR), quantitative RT-PCR, and Affymetrix oligonucleotide microarrays. DD identified eight differentially expressed cDNAs, including inhibitor of apoptosis-1, 2′-5′ oligoadenylate synthetase (OAS), a 2′-5′ OAS-like (OASL) gene, galectin-9, myxovirus protein A (MxA), regulator of G-protein signaling, endothelial and smooth muscle cell-derived neuropilin-like protein, and phospholipid scramblase 1. Microarray analysis of 22,000 human genes confirmed these findings and identified an additional 269 genes that were induced and 126 that were repressed more than fourfold after DV infection. Broad functional responses that were activated included the stress, defense, immune, cell adhesion, wounding, inflammatory, and antiviral pathways. These changes in gene expression were seen after infection of HUVECs with either laboratory-adapted virus or with virus isolated directly from plasma of DV-infected patients. Tumor necrosis factor alpha, OASL, and MxA and h-IAP1 genes were induced within the first 8 to 12 h after infection, suggesting a direct effect of DV infection. These global analyses of DV effects on cellular gene expression identify potentially novel mechanisms involved in dengue disease manifestations such as hemostatic disturbance.

Abstract 103: MiR-4261 Controls Endothelial Cells Angiogenesis

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Qiulian Zhou ◽  
Dongchao Lv ◽  
Qi Sun ◽  
Ping Chen ◽  
Yihua Bei ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Heart Diseases ◽  
Umbilical Vein ◽  
Tissue Perfusion ◽  
Tube Formation ◽  
Artery Disease ◽  
Incorporation Assay ◽  
Umbilical Vein Endothelial Cells

Myocardial infarction (MI) is among major causes of morbidity and mortality associated with coronary artery disease. Angiogenesis improves tissue perfusion and cardiac repair after MI. Therefore, angiogenesis is considered to be a novel therapeutic way for ischemic heart diseases. MicroRNAs (miRNAs, miRs) have been reported to play important roles in regulating post-ischemic neovascularization. The current study aims at investigating the role of miR-4261 in angiogenesis. We found that miR-4261 mimics increased, while miR-4261 inhibitors decreased the proliferation of human umbilical vein endothelial cells (HUVEC) using EdU incorporation assay (17.25%±1.31% vs 30.91%±0.92% in nc-mimics vs mir-4261-mimics, 17.91%±1.36% vs 8.51%±0.82% in nc-inhibitor vs mir-4261-inhibitor, respectively) and CCK-8 assays (0.84±0.04 vs 1.38±0.04 in nc-mimics vs mir-4261-mimics, 0.80±0.02 vs 0.72±0.01 in nc-inhibitor vs mir-4261-inhibitor, respectively). The wound healing assay showed that miR-4261 mimic transfection resulted in a significant increase in the migration of HUVEC compared to that of the negative controls while miR-4261 inhibition had the opposite effects. Tube formation assays showed that HUVEC transfected with miR-4261 mimics increased the number of tubes formed (57.25±2.56 vs 81.5±2.53 in nc-mimics vs mir-4261-mimics, respectively), while miR-4261 inhibitor-transfected cells had the opposite effect (56.55±0.45 vs 41.38±0.52 in nc-inhibitor vs mir-4261-inhibitor, respectively). These results indicate that miR-4261 play an important role in regulating angiogenesis. However, it remains unknown which target gene mediated the effects of miR-4261. Thus, it will be of great interest to further investigate the molecular mechanisms of miR-4261 in the proliferation, migration, and tube formation of HUVEC in vitro. MiR-4261 could be a potential therapeutic target to enhance angiogenesis.

scholarly journals Hypoxic human umbilical vein endothelial cells induce activation of adherent polymorphonuclear leukocytes

Blood ◽  
1994 ◽  
Vol 83 (12) ◽  
pp. 3705-3716 ◽  
Author(s):  
T Arnould ◽  
C Michiels ◽  
J Remacle
Keyword(s):  
Endothelial Cells ◽  
Superoxide Dismutase ◽  
Superoxide Anion ◽  
Calcium Concentration ◽  
Molecular Mechanisms ◽  
Umbilical Vein ◽  
Superoxide Anion Production ◽  
Elastase Inhibitor ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Abstract Several pieces of evidence are reported for the accumulation of activated neutrophils in ischemic and reperfused tissues leading to the transformation of the ischemic tissue into an inflammatory territory and to an enhancement of tissue damages during reoxygenation. However, the molecular mechanisms responsible for these observations and the precise role played by endothelial cells in this process are still poorly understood. In this study, an in vitro model that mimics this situation was used to investigate the effects of hypoxia-incubated human umbilical vein endothelial cells (HUVEC) on polymorphonuclear leukocyte (PMN) functions. A strong PMN activation characterized by an increase in intracellular calcium concentration as well as by superoxide anion release and leukotriene B4 production was observed when these cells were coincubated with hypoxic HUVEC. On the other hand, conditioned medium from hypoxia-incubated HUVEC failed to activate PMN, as determined by the lack of PMN calcium concentration increase, the failure of superoxide anion production enhancement, as well as the absence of effects on the integrin CD18, CD11a, and CD11b expression. These results indicate that the presence of hypoxia- incubated HUVEC is necessary to obtain an activation of the PMN, probably via the adherence process. Once activated by coincubation with hypoxic HUVEC, PMN became cytotoxic, as evidenced by 51Cr released from prelabeled HUVEC. This cytotoxic effect of activated PMN for hypoxic endothelial cells could be prevented by a combination of superoxide dismutase and catalase (94% inhibition), whereas superoxide dismutase alone was inefficient. Antiprotease (alpha 2-macroglobulin) and a specific elastase inhibitor (MAAPV-CMK) were also inefficient. These results correlate very well with the fact that no increase in elastase release could be observed in supernatants from PMN coincubated with hypoxic HUVEC. Furthermore, when adherence process was blocked by oleic acid or by anti-ICAM-1 monoclonal antibodies, protection was, respectively, 90% and 72%. We thus evidenced that free radicals but not elastase released from activated PMN coincubated with hypoxic HUVEC are involved in HUVEC injury. We conclude from these results that PMN activation is initiated by PMN adherence to hypoxic HUVEC. These observations indicate that hypoxic HUVEC may be partly responsible for neutrophil activation observed in ischemic tissues, which is part of the amplification process of tissue damage.

scholarly journals In vitro effects of low-level aldehyde exposures on human umbilical vein endothelial cells

2015 ◽  
Vol 4 (5) ◽  
pp. 1250-1259 ◽  
Author(s):  
Nuan P. Cheah ◽  
Jeroen L.A. Pennings ◽  
Jolanda P. Vermeulen ◽  
Roger W.L. Godschalk ◽  
Frederik J. van Schooten ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Tobacco Smoke ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
In Vitro Effects ◽  
Umbilical Vein Endothelial Cells ◽  
Disease Exposure

Aldehydes cause gene expression changes for genes associated with cardiovascular disease. Exposure to aldehydes from tobacco smoke needs to be controlled.

Comparative analysis of effects of cyclic uniaxial and equiaxial stretches on gene expression of human umbilical vein endothelial cells

2015 ◽  
Vol 39 (6) ◽  
pp. 741-749 ◽  
Author(s):  
Shahrokh Shojaei ◽  
Mohammad Tafazzoli-Shahdpour ◽  
Mohammad Ali Shokrgozar ◽  
Nooshin Haghighipour
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Comparative Analysis ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

The Influence of Cyclic and Uniform Shear Stresses Concurrent with Cyclic Stretch on the Gene Expression of Human Umbilical Vein Endothelial Cells

2013 ◽  
Vol 3 (6) ◽  
pp. 673-678 ◽  
Author(s):  
Shahrokh Shojaei ◽  
Mohammad Tafazzoli-Shadpour ◽  
Mohammad Ali Shokrgozar ◽  
Nooshin Haghighipour ◽  
Najmeh Safaei ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Cyclic Stretch ◽  
Shear Stresses ◽  
Human Umbilical Vein ◽  
Uniform Shear ◽  
Umbilical Vein Endothelial Cells

scholarly journals Microcystins Induces Vascular Inflammation in Human Umbilical Vein Endothelial Cells via Activation of NF-κB

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jun Shi ◽  
Jie Zhou ◽  
Min Zhang
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Inflammatory Process ◽  
Molecular Mechanisms ◽  
Umbilical Vein ◽  
Health Hazard ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Microcystins (MCs) produced by toxic cyanobacteria cause serious water pollution and public health hazard to humans and animals. However, direct molecular mechanisms of MC-LR in vascular endothelial cells (ECs) have not been understood yet. In this study, we investigated whether MC-LR induces vascular inflammatory process in cultured human umbilical vein endothelial cells (HUVECs). Our data demonstrated that MC-LR decreased HUVECs proliferation and tube formation and enhanced apoptosis. MC-LR also induced intracellular reactive oxygen species formation (ROS) in HUVECs. The MC-LR directly stimulated phosphorylation of NF-κB. Furthermore, MC-LR also increased cell adhesion molecules (ICAM-1 and VCAM-1) expression in HUVECs. Taken together, the present data suggested that MC-LR induced vascular inflammatory process, which may be closely related to the oxidative stress, NF-κB activation, and cell adhesion molecules expression in HUVECs. Our findings may highlight that MC-LR causes potential damage to blood vessels.

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